Reference Citation Analysis: Find an Article, Find a Category, Find a Journal, Find a Scholar

For: Takami S, Yamashita S, Kihara S, Ishigami M, Takemura K, Kume N, Kita T, Matsuzawa Y. Lipoprotein(a) enhances the expression of intercellular adhesion molecule-1 in cultured human umbilical vein endothelial cells. Circulation 1998;97:721-8. [PMID: 9498534 DOI: 10.1161/01.cir.97.8.721] [Citation(s) in RCA: 74] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]

For:	Takami S, Yamashita S, Kihara S, Ishigami M, Takemura K, Kume N, Kita T, Matsuzawa Y. Lipoprotein(a) enhances the expression of intercellular adhesion molecule-1 in cultured human umbilical vein endothelial cells. Circulation 1998;97:721-8. [PMID: 9498534 DOI: 10.1161/01.cir.97.8.721] [Citation(s) in RCA: 74] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023]

Number

Cited by Other Article(s)

Mauriello A, Correra A, Maratea AC, Caturano A, Liccardo B, Perrone MA, Giordano A, Nigro G, D’Andrea A, Russo V. Serum Lipids, Inflammation, and the Risk of Atrial Fibrillation: Pathophysiological Links and Clinical Evidence. J Clin Med 2025;14:1652. [PMID: 40095683 PMCID: PMC11899858 DOI: 10.3390/jcm14051652] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/20/2025] [Revised: 02/13/2025] [Accepted: 02/27/2025] [Indexed: 03/19/2025] Open

Affiliation(s)

Alfredo Mauriello Cardiology Unit, Department of Medical and Translational Sciences, University of Campania “Luigi Vanvitelli”, Monaldi Hospital, 80131 Naples, Italy; (A.M.); (A.C.M.); (B.L.); (G.N.) Cardiology and Intensive Care Unit, Department of Cardiology, “Umberto I” Hospital, 84014 Nocera Inferiore, Italy; Intensive Cardiac Care Unit, “San Giuseppe Moscati” Hospital, ASL Caserta 81031 Aversa, Italy;
Adriana Correra Intensive Cardiac Care Unit, “San Giuseppe Moscati” Hospital, ASL Caserta 81031 Aversa, Italy;
Anna Chiara Maratea Cardiology Unit, Department of Medical and Translational Sciences, University of Campania “Luigi Vanvitelli”, Monaldi Hospital, 80131 Naples, Italy; (A.M.); (A.C.M.); (B.L.); (G.N.)
Alfredo Caturano Internal Medicine Unit, Department of Advanced Medical and Surgical Sciences, University of Campania Luigi Vanvitelli, Piazza Luigi Miraglia 2, 80138 Naples, Italy;
Biagio Liccardo Cardiology Unit, Department of Medical and Translational Sciences, University of Campania “Luigi Vanvitelli”, Monaldi Hospital, 80131 Naples, Italy; (A.M.); (A.C.M.); (B.L.); (G.N.)
Marco Alfonso Perrone Department of Cardiology and CardioLab, University of Rome Tor Vergata, 00133 Rome, Italy;
Antonio Giordano Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA;
Gerardo Nigro Cardiology Unit, Department of Medical and Translational Sciences, University of Campania “Luigi Vanvitelli”, Monaldi Hospital, 80131 Naples, Italy; (A.M.); (A.C.M.); (B.L.); (G.N.)
Antonello D’Andrea Cardiology and Intensive Care Unit, Department of Cardiology, “Umberto I” Hospital, 84014 Nocera Inferiore, Italy;
Vincenzo Russo Cardiology Unit, Department of Medical and Translational Sciences, University of Campania “Luigi Vanvitelli”, Monaldi Hospital, 80131 Naples, Italy; (A.M.); (A.C.M.); (B.L.); (G.N.) Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA;

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Lian PA, Zhu WQ, Zhao WX, Huang PP, Ran JL, Tang YX, Huang XS, Li R. Lipoprotein(a) in atherosclerotic cardiovascular disease and proprotein convertase subtilisin/kexin-type 9 inhibitors. Clin Chim Acta 2025;565:119982. [PMID: 39366516 DOI: 10.1016/j.cca.2024.119982] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/08/2024] [Revised: 09/28/2024] [Accepted: 09/29/2024] [Indexed: 10/06/2024]

Qin T, Ma TY, Huang K, Lu SJ, Zhong JH, Li JJ. Lipoprotein (a)-Related Inflammatory Imbalance: A Novel Horizon for the Development of Atherosclerosis. Curr Atheroscler Rep 2024;26:383-394. [PMID: 38878139 PMCID: PMC11236888 DOI: 10.1007/s11883-024-01215-5] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 05/15/2024] [Indexed: 07/11/2024]

Pavlatos N, Kalra DK. The Role of Lipoprotein(a) in Peripheral Artery Disease. Biomedicines 2024;12:1229. [PMID: 38927436 PMCID: PMC11200468 DOI: 10.3390/biomedicines12061229] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/05/2024] [Revised: 05/25/2024] [Accepted: 05/29/2024] [Indexed: 06/28/2024] Open

Groenen AG, Matveyenko A, Matienzo N, Halmos B, Zhang H, Westerterp M, Reyes-Soffer G. Apolipoprotein(a) production and clearance are associated with plasma IL-6 and IL-18 levels, dependent on ethnicity. Atherosclerosis 2024;391:117474. [PMID: 38428286 DOI: 10.1016/j.atherosclerosis.2024.117474] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/19/2023] [Revised: 01/31/2024] [Accepted: 02/01/2024] [Indexed: 03/03/2024]

Liu Y, Wang R, Li S, Zhang C, Lip GYH, Thabane L, Li G. Relationship Between Lipoprotein(a), Renal Function Indicators, and Chronic Kidney Disease: Evidence From a Large Prospective Cohort Study. JMIR Public Health Surveill 2024;10:e50415. [PMID: 38294877 PMCID: PMC10867749 DOI: 10.2196/50415] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/29/2023] [Revised: 12/05/2023] [Accepted: 01/03/2024] [Indexed: 02/01/2024] Open

Abstract

BACKGROUND

Chronic kidney disease (CKD) poses a significant global public health challenge. While lipoprotein(a) (Lp[a]) has been established as a significant factor in cardiovascular disease, its connection to CKD risk remains a topic of debate. Existing evidence indicates diverse risks of kidney disease among individuals with various renal function indicators, even when within the normal range.

OBJECTIVE

This study aims to investigate the joint associations between different renal function indicators and Lp(a) regarding the risks of incident CKD in the general population.

METHODS

The analysis involved a cohort of 329,415 participants without prior CKD who were enrolled in the UK Biobank between 2006 and 2010. The participants, with an average age of 56 (SD 8.1) years, included 154,298/329,415 (46.84%) males. At baseline, Lp(a) levels were measured using an immunoturbidimetric assay and classified into 2 groups: low (<75 nmol/L) and high (≥75 nmol/L). To assess participants' baseline renal function, we used the baseline urine albumin-to-creatinine ratio (UACR) and estimated glomerular filtration rate (eGFR). The relationship between Lp(a), renal function indicators, and the risk of CKD was evaluated using multivariable Cox regression models. These models were adjusted for various factors, including sociodemographic variables, lifestyle factors, comorbidities, and laboratory measures.

RESULTS

A total of 6003 incident CKD events were documented over a median follow-up period of 12.5 years. The association between elevated Lp(a) levels and CKD risk did not achieve statistical significance among all participants, with a hazard ratio (HR) of 1.05 and a 95% CI ranging from 0.98 to 1.13 (P=.16). However, a notable interaction was identified between Lp(a) and UACR in relation to CKD risk (P for interaction=.04), whereas no significant interaction was observed between Lp(a) and eGFR (P for interaction=.96). When compared with the reference group with low Lp(a) and low-normal UACR (<10 mg/g), the group with high Lp(a) and low-normal UACR exhibited a nonsignificant association with CKD risk (HR 0.98, 95% CI 0.90-1.08; P=.74). By contrast, both the low Lp(a) and high-normal UACR (≥10 mg/g) group (HR 1.16, 95% CI 1.08-1.24; P<.001) and the high Lp(a) and high-normal UACR group (HR 1.32, 95% CI 1.19-1.46; P<.001) demonstrated significant associations with increased CKD risks. In individuals with high-normal UACR, elevated Lp(a) was linked to a significant increase in CKD risk, with an HR of 1.14 and a 95% CI ranging from 1.03 to 1.26 (P=.01). Subgroup analyses and sensitivity analyses consistently produced results that were largely in line with the main findings.

CONCLUSIONS

The analysis revealed a significant interaction between Lp(a) and UACR in relation to CKD risk. This implies that Lp(a) may act as a risk factor for CKD even when considering UACR. Our findings have the potential to provide valuable insights into the assessment and prevention of CKD, emphasizing the combined impact of Lp(a) and UACR from a public health perspective within the general population. This could contribute to enhancing public awareness regarding the management of Lp(a) for the prevention of CKD.

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Brosolo G, Da Porto A, Marcante S, Picci A, Capilupi F, Capilupi P, Bulfone L, Vacca A, Bertin N, Vivarelli C, Comand J, Catena C, Sechi LA. Lipoprotein(a): Just an Innocent Bystander in Arterial Hypertension? Int J Mol Sci 2023;24:13363. [PMID: 37686169 PMCID: PMC10487946 DOI: 10.3390/ijms241713363] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/07/2023] [Revised: 08/25/2023] [Accepted: 08/25/2023] [Indexed: 09/10/2023] Open

Affiliation(s)

Gabriele Brosolo Department of Medicine, University of Udine, 33100 Udine, Italy; (A.D.P.); (S.M.); (A.P.); (F.C.); (P.C.); (L.B.); (A.V.); (N.B.); (C.V.); (J.C.); (C.C.) European Hypertension Excellence Center, Clinica Medica, University of Udine, 33100 Udine, Italy
Andrea Da Porto Department of Medicine, University of Udine, 33100 Udine, Italy; (A.D.P.); (S.M.); (A.P.); (F.C.); (P.C.); (L.B.); (A.V.); (N.B.); (C.V.); (J.C.); (C.C.) Diabetes and Metabolism Unit, Clinica Medica, University of Udine, 33100 Udine, Italy
Stefano Marcante Department of Medicine, University of Udine, 33100 Udine, Italy; (A.D.P.); (S.M.); (A.P.); (F.C.); (P.C.); (L.B.); (A.V.); (N.B.); (C.V.); (J.C.); (C.C.) European Hypertension Excellence Center, Clinica Medica, University of Udine, 33100 Udine, Italy
Alessandro Picci Department of Medicine, University of Udine, 33100 Udine, Italy; (A.D.P.); (S.M.); (A.P.); (F.C.); (P.C.); (L.B.); (A.V.); (N.B.); (C.V.); (J.C.); (C.C.) European Hypertension Excellence Center, Clinica Medica, University of Udine, 33100 Udine, Italy
Filippo Capilupi Department of Medicine, University of Udine, 33100 Udine, Italy; (A.D.P.); (S.M.); (A.P.); (F.C.); (P.C.); (L.B.); (A.V.); (N.B.); (C.V.); (J.C.); (C.C.) European Hypertension Excellence Center, Clinica Medica, University of Udine, 33100 Udine, Italy
Patrizio Capilupi Department of Medicine, University of Udine, 33100 Udine, Italy; (A.D.P.); (S.M.); (A.P.); (F.C.); (P.C.); (L.B.); (A.V.); (N.B.); (C.V.); (J.C.); (C.C.) European Hypertension Excellence Center, Clinica Medica, University of Udine, 33100 Udine, Italy
Luca Bulfone Department of Medicine, University of Udine, 33100 Udine, Italy; (A.D.P.); (S.M.); (A.P.); (F.C.); (P.C.); (L.B.); (A.V.); (N.B.); (C.V.); (J.C.); (C.C.) European Hypertension Excellence Center, Clinica Medica, University of Udine, 33100 Udine, Italy
Antonio Vacca Department of Medicine, University of Udine, 33100 Udine, Italy; (A.D.P.); (S.M.); (A.P.); (F.C.); (P.C.); (L.B.); (A.V.); (N.B.); (C.V.); (J.C.); (C.C.) European Hypertension Excellence Center, Clinica Medica, University of Udine, 33100 Udine, Italy
Nicole Bertin Department of Medicine, University of Udine, 33100 Udine, Italy; (A.D.P.); (S.M.); (A.P.); (F.C.); (P.C.); (L.B.); (A.V.); (N.B.); (C.V.); (J.C.); (C.C.) Thrombosis and Hemostasis Unit, Clinica Medica, University of Udine, 33100 Udine, Italy
Cinzia Vivarelli Department of Medicine, University of Udine, 33100 Udine, Italy; (A.D.P.); (S.M.); (A.P.); (F.C.); (P.C.); (L.B.); (A.V.); (N.B.); (C.V.); (J.C.); (C.C.)
Jacopo Comand Department of Medicine, University of Udine, 33100 Udine, Italy; (A.D.P.); (S.M.); (A.P.); (F.C.); (P.C.); (L.B.); (A.V.); (N.B.); (C.V.); (J.C.); (C.C.) European Hypertension Excellence Center, Clinica Medica, University of Udine, 33100 Udine, Italy
Cristiana Catena Department of Medicine, University of Udine, 33100 Udine, Italy; (A.D.P.); (S.M.); (A.P.); (F.C.); (P.C.); (L.B.); (A.V.); (N.B.); (C.V.); (J.C.); (C.C.) European Hypertension Excellence Center, Clinica Medica, University of Udine, 33100 Udine, Italy
Leonardo A. Sechi Department of Medicine, University of Udine, 33100 Udine, Italy; (A.D.P.); (S.M.); (A.P.); (F.C.); (P.C.); (L.B.); (A.V.); (N.B.); (C.V.); (J.C.); (C.C.) European Hypertension Excellence Center, Clinica Medica, University of Udine, 33100 Udine, Italy Diabetes and Metabolism Unit, Clinica Medica, University of Udine, 33100 Udine, Italy Thrombosis and Hemostasis Unit, Clinica Medica, University of Udine, 33100 Udine, Italy

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Mechanism of oxidized phospholipid-related inflammatory response in vascular ageing. Ageing Res Rev 2023;86:101888. [PMID: 36806379 DOI: 10.1016/j.arr.2023.101888] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/21/2022] [Revised: 02/05/2023] [Accepted: 02/16/2023] [Indexed: 02/20/2023]

Lampsas S, Xenou M, Oikonomou E, Pantelidis P, Lysandrou A, Sarantos S, Goliopoulou A, Kalogeras K, Tsigkou V, Kalpis A, Paschou SA, Theofilis P, Vavuranakis M, Tousoulis D, Siasos G. Lipoprotein(a) in Atherosclerotic Diseases: From Pathophysiology to Diagnosis and Treatment. Molecules 2023;28:969. [PMID: 36770634 PMCID: PMC9918959 DOI: 10.3390/molecules28030969] [Citation(s) in RCA: 7] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/23/2022] [Revised: 01/12/2023] [Accepted: 01/17/2023] [Indexed: 01/21/2023] Open

Affiliation(s)

Stamatios Lampsas 3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 11527 Athens, Greece
Maria Xenou 3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 11527 Athens, Greece
Evangelos Oikonomou 3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 11527 Athens, Greece
Panteleimon Pantelidis 3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 11527 Athens, Greece
Antonios Lysandrou 3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 11527 Athens, Greece
Savvas Sarantos 3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 11527 Athens, Greece
Athina Goliopoulou 3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 11527 Athens, Greece
Konstantinos Kalogeras 3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 11527 Athens, Greece 1st Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Hippokration General Hospital, 11527 Athens, Greece
Vasiliki Tsigkou 3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 11527 Athens, Greece
Athanasios Kalpis 3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 11527 Athens, Greece
Stavroula A. Paschou 1st Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Hippokration General Hospital, 11527 Athens, Greece
Panagiotis Theofilis 3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 11527 Athens, Greece
Manolis Vavuranakis 3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 11527 Athens, Greece
Dimitris Tousoulis 1st Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Hippokration General Hospital, 11527 Athens, Greece
Gerasimos Siasos 3rd Department of Cardiology, National and Kapodistrian University of Athens, Medical School, Sotiria Chest Disease Hospital, 11527 Athens, Greece Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA

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Dimitroglou Y, Aggeli C, Theofilis P, Tsioufis P, Oikonomou E, Tsioufis K, Tousoulis D. Lipoprotein(a) as a Predictive Biomarker and Therapeutic Target for Acute Coronary Syndromes. Curr Pharm Des 2023;29:1835-1843. [PMID: 37264657 DOI: 10.2174/1381612829666230601155001] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/29/2023] [Revised: 04/05/2023] [Accepted: 05/03/2023] [Indexed: 06/03/2023]

Simantiris S, Antonopoulos AS, Papastamos C, Benetos G, Koumallos N, Tsioufis K, Tousoulis D. Lipoprotein(a) and inflammation- pathophysiological links and clinical implications for cardiovascular disease. J Clin Lipidol 2023;17:55-63. [PMID: 36333256 DOI: 10.1016/j.jacl.2022.10.004] [Citation(s) in RCA: 19] [Impact Index Per Article: 9.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/13/2022] [Revised: 10/11/2022] [Accepted: 10/12/2022] [Indexed: 11/05/2022]

Wang A, Zhang S, Li Y, Zhu F, Xie B. Study on the relationship between lipoprotein (a) and diabetic kidney disease. J Diabetes Complications 2023;37:108378. [PMID: 36549039 DOI: 10.1016/j.jdiacomp.2022.108378] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/04/2022] [Revised: 11/29/2022] [Accepted: 12/01/2022] [Indexed: 12/23/2022]

Abstract

OBJECTIVE

Little is currently known about the role of lipid metabolism in diabetic kidney disease (DKD), warranting further study. The present study sought to investigate the correlation between lipid metabolism and renal function as well as renal pathological grade/score in DKD patients.

METHODS

A total of 224 patients diagnosed with DKD by pathological examination were retrospectively analyzed, of which 74 patients were further evaluated by DKD pathological grade/score. ANOVA was used to investigate serum lipoprotein (a) [Lp (a)] levels in DKD patients with different chronic kidney disease (CKD) stages. Spearman correlation analysis was used to evaluate the relationship between Lp (a) and renal function-related indicators. The DKD pathological grade/score was also evaluated with this method. The receiver operating characteristic (ROC) curve was used to analyze the value of Lp (a) in assessing renal function and pathological changes.

RESULTS

There were significant differences in Lp (a) levels among different CKD stages (H = 17.063, p = 0.002) and glomerular grades (H = 12.965, p = 0.005). Lp (a) levels correlated with serum creatinine (p = 0.000), blood urea nitrogen (p = 0.000), estimated glomerular filtration rate (p = 0.000), 24-h proteinuria (24hUPro, p = 0.000), urine microalbumin (p = 0.000), urine albumin creatinine ratio (p = 0.000), glomerular basement membrane thickness (p = 0.003), and glomerular grade (p = 0.039). ROC curve demonstrated good performance of Lp (a) as an indicator to assess CKD stage 4-5 (AUC = 0.684, p = 0.000), 24hUPro > 3.5 g (AUC = 0.720, p = 0.000), and glomerular grade III-IV (AUC = 0.695, p = 0.012).

CONCLUSIONS

Elevated levels of Lp (a) are associated with decreased GFR, increased proteinuria, and renal pathological progression, suggesting they could be used to monitor changes in DKD patients.

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Naito R, Daida H, Masuda D, Harada-Shiba M, Arai H, Bujo H, Ishibashi S, Koga N, Oikawa S, Yamashita S. Relation of Serum Lipoprotein(a) Levels to Lipoprotein and Apolipoprotein Profiles and Atherosclerotic Diseases in Japanese Patients with Heterozygous Familial Hypercholesterolemia: Familial Hypercholesterolemia Expert Forum (FAME) Study. J Atheroscler Thromb 2022;29:1188-1200. [PMID: 34456199 PMCID: PMC9371754 DOI: 10.5551/jat.63019] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/06/2021] [Accepted: 07/27/2021] [Indexed: 11/11/2022] Open

Dzobo KE, Kraaijenhof JM, Stroes ES, Nurmohamed NS, Kroon J. Lipoprotein(a): An underestimated inflammatory mastermind. Atherosclerosis 2022;349:101-109. [DOI: 10.1016/j.atherosclerosis.2022.04.004] [Citation(s) in RCA: 11] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/16/2021] [Revised: 02/09/2022] [Accepted: 04/01/2022] [Indexed: 12/11/2022]

Kraaijenhof JM, Hovingh GK, Stroes ES, Kroon J. The iterative lipid impact on inflammation in atherosclerosis. Curr Opin Lipidol 2021;32:286-292. [PMID: 34392272 PMCID: PMC8452331 DOI: 10.1097/mol.0000000000000779] [Citation(s) in RCA: 12] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/24/2022]

Beyond Lipoprotein(a) plasma measurements: Lipoprotein(a) and inflammation. Pharmacol Res 2021;169:105689. [PMID: 34033878 PMCID: PMC9247870 DOI: 10.1016/j.phrs.2021.105689] [Citation(s) in RCA: 48] [Impact Index Per Article: 12.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/09/2021] [Revised: 05/18/2021] [Accepted: 05/19/2021] [Indexed: 12/20/2022]

Chang NC, Yeh CT, Lin YK, Kuo KT, Fong IH, Kounis NG, Hu P, Hung MY. Garcinol Attenuates Lipoprotein(a)-Induced Oxidative Stress and Inflammatory Cytokine Production in Ventricular Cardiomyocyte through α7-Nicotinic Acetylcholine Receptor-Mediated Inhibition of the p38 MAPK and NF-κB Signaling Pathways. Antioxidants (Basel) 2021;10:antiox10030461. [PMID: 33809417 PMCID: PMC8000018 DOI: 10.3390/antiox10030461] [Citation(s) in RCA: 16] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/28/2021] [Revised: 02/27/2021] [Accepted: 03/10/2021] [Indexed: 12/12/2022] Open

Abstract

Garcinol, a nicotinic acetylcholine receptor (nAChR) antagonist, has recently been established as an anti-inflammation agent. However, the molecular mechanism by which garcinol suppresses inflammation in the context of acute myocardial infarction (AMI) remains unclear. Hypothesis: We hypothesized that the administration of physiological doses of garcinol in mice with isoproterenol-induced AMI decreased the effect of lipoprotein(a) (Lp(a))-induced inflammation both in vivo and in vitro via the α7-nAChRs mediated p38 mitogen-activated protein kinase (MAPK)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) signaling pathway. We analyzed altered reactive oxygen species (ROS) generation, the production of superoxide by mitochondria, cytokine expression patterns, and the role of the p38 MAPK/NF-κB signaling pathway after Lp(a)-stimulated human ventricular cardiomyocyte AC16 cells were treated with increasing doses of garcinol. C-reactive protein (CRP), interleukin (IL)-1β, IL-6, or tumor necrosis factor (TNF)-α production were detected by enzyme-linked immunosorbent assay. The Cell Counting Kit-8 assay was used to evaluate drug cytotoxicity. Western blots and confocal fluorescence microscopy were used to determine altered expression patterns of inflammatory biomarkers. We also examined whether the therapeutic effect of garcinol in AMI was mediated in part by α7-nAChR. Lp(a)-induced inflammatory cardiomyocytes had increased expression of membrane-bound α7-nAChRs in vitro and in vivo. Low-dose garcinol did not affect cardiomyocyte viability but significantly reduced mitochondrial ROS, CRP, IL-1β, IL-6, and TNF-α production in Lp(a)-stimulated cardiomyocytes (p < 0.05). The Lp(a)-induced phosphorylation of p38 MAPKs, CamKII, and NFκB, as well as NFκB-p65 nuclear translocation, was also suppressed (p < 0.05) by garcinol, while the inhibition of p38 MAPK by the inhibitor SB203580 decreased the phosphorylation of extracellular signal-regulated kinase (ERK) and p38 MAPK. Garcinol protected cardiomyocytes by inhibiting apoptosis and inflammation in mice with AMI. Furthermore, garcinol also enhanced the expression of microRNA-205 that suppressed the α7-nAChR-induced p38 MAPK/NF-κB signaling pathway. Garcinol suppresses Lp(a)-induced oxidative stress and inflammatory cytokines by α7-nAChR-mediated inhibition of p38 MAPK/NF-κB signaling in cardiomyocyte AC16 cells and isoproterenol-induced AMI mice.

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Affiliation(s)

Nen-Chung Chang Division of Cardiology, Department of Internal Medicine, Taipei Medical University Hospital, Taipei 110, Taiwan Division of Cardiology, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan; Taipei Heart Institute, Taipei Medical University, Taipei 110, Taiwan
Chi-Tai Yeh Department of Medical Research and Education, Taipei Medical University—Shuang Ho Hospital, New Taipei City 23561, Taiwan; (C.-T.Y.); (I.-H.F.) Department of Medical Laboratory Science and Biotechnology, Yuanpei University of Medical Technology, Hsinchu City 30015, Taiwan
Yen-Kuang Lin Biostatistics Center, Office of Data Science, Taipei Medical University, Taipei 110, Taiwan Graduate Institute of Data Science, Taipei Medical University, Taipei 110, Taiwan Research Center of Big Data, College of Management, Taipei Medical University, Taipei 110, Taiwan;
Kuang-Tai Kuo Division of Thoracic Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City 23561, Taiwan; Division of Thoracic Surgery, Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan
Iat-Hang Fong Department of Medical Research and Education, Taipei Medical University—Shuang Ho Hospital, New Taipei City 23561, Taiwan; (C.-T.Y.); (I.-H.F.) Department of Medical Laboratory Science and Biotechnology, Yuanpei University of Medical Technology, Hsinchu City 30015, Taiwan
Nicholas G. Kounis Department of Internal Medicine, Division of Cardiology, University of Patras Medical School, 26221 Patras, Greece;
Patrick Hu Department of Cardiology, University of California, Riverside, CA 92521, USA; Department of Cardiology, Riverside Medical Clinic, Riverside, CA 92506, USA
Ming-Yow Hung Division of Cardiology, Department of Internal Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei 110, Taiwan; Taipei Heart Institute, Taipei Medical University, Taipei 110, Taiwan Division of Cardiology, Department of Internal Medicine, Shuang Ho Hospital, Taipei Medical University, New Taipei City 23561, Taiwan Correspondence: ; Tel.: +886-2-22490088

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Huded CP, Shah NP, Puri R, Nicholls SJ, Wolski K, Nissen SE, Cho L. Association of Serum Lipoprotein (a) Levels and Coronary Atheroma Volume by Intravascular Ultrasound. J Am Heart Assoc 2020;9:e018023. [PMID: 33222598 PMCID: PMC7763761 DOI: 10.1161/jaha.120.018023] [Citation(s) in RCA: 20] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/28/2022]

Abstract

Background

Lp(a) (lipoprotein (a)) is a risk factor for cardiovascular events, but the mechanism of increased risk is uncertain. This study evaluated the relationship between Lp(a) and coronary atheroma volume by intravascular ultrasound.

Methods and Results

This was a post hoc analysis of 6 randomized trials of coronary atheroma by intravascular ultrasound. The population was stratified into high (≥60 mg/dL) and low (<60 mg/dL) baseline serum Lp(a). The primary outcome was baseline coronary percent atheroma volume. A mixed model adjusted for baseline low density lipoprotein, ApoB (apoliporotein B100), non‐high density lipoprotein, sex, age, race, history of myocardial infarction, statin use, and intravascular ultrasound study was used to provide estimates of baseline plaque burden. Of 3943 patients, 17.3% (683) had Lp(a) ≥ 60 mg/dL and 82.7% (3260) had Lp(a) < 60 mg/dL. At baseline, uncorrected low density lipoprotein level (107.7 ± 32.0 versus 99.1 ± 31.5) and statin therapy (99.0% versus 97.0%) were higher in patients with high Lp(a) levels, but low density lipoprotein corrected for Lp(a) was lower (80.6 ± 32.0 versus 94.0 ± 31.4) in patients with high Lp(a) levels. Percent atheroma volume was significantly higher in the high Lp(a) group in unadjusted (38.2% [32.8, 43.6] versus 37.1% [31.4, 43.1], P=0.01) and risk‐adjusted analyses (38.7%±0.5 versus 37.5%±0.5, P<0.001). There was a significant association of increasing risk‐adjusted percent atheroma volume across quintiles of Lp(a) (Lp(a) quintiles 1‐5; 37.3 ± 0.5%, 37.2 ± 0.5%, 37.3 ± 0.5%, 38.0 ± 0.5%, 38.5 ± 0.5%, P=0.002).

Conclusions

Elevated Lp(a) is independently associated with increased percent atheroma volume. Further work is needed to clarify the relationship of Lp(a)‐lowering treatment with cardiovascular outcomes.

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Geng J, Fu W, Yu X, Lu Z, Liu Y, Sun M, Yu P, Li X, Fu L, Xu H, Sui D. Ginsenoside Rg3 Alleviates ox-LDL Induced Endothelial Dysfunction and Prevents Atherosclerosis in ApoE^-/- Mice by Regulating PPARγ/FAK Signaling Pathway. Front Pharmacol 2020;11:500. [PMID: 32390845 PMCID: PMC7188907 DOI: 10.3389/fphar.2020.00500] [Citation(s) in RCA: 30] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/26/2019] [Accepted: 03/30/2020] [Indexed: 12/14/2022] Open

Abstract

The initiation of atherosclerosis (AS) induced by dyslipidemia is accompanied by endothelial dysfunction, including decreased healing ability and increased recruitment of monocytes. Studies showed ginsenoside Rg3 has potential to treat diseases associated with endothelial dysfunction which can protects against antineoplastic drugs induced cardiotoxicity by repairing endothelial function, while the effect and mechanism of Rg3 on dyslipidemia induced endothelial dysfunction and AS are not clear. Therefore, we investigated the effects of Rg3 on oxidized low-density lipoprotein (ox-LDL) induced human umbilical vein endothelial cells (HUVECs) dysfunction and high-fat diets (HFD) induced atherosclerosis in ApoE^−/− mice, as well as the mechanism. For in vitro assay, Rg3 enhanced healing of HUVECs and inhibited human monocytes (THP-1) adhesion to HUVECs disturbed by ox-LDL, down-regulated focal adhesion kinase (FAK)-mediated expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1); restrained the FAK-mediated non-adherent dependent pathway containing matrix metalloproteinase (MMP)-2/9 expression, activation of nuclear factor-kappa B (NF-κB), high mRNA levels of monocyte chemotactic protein 1 (MCP-1) and interleukin 6 (IL-6), besides Rg3 up-regulated peroxisome proliferators-activated receptor γ (PPARγ) in ox-LDL-stimulated HUVECs. GW9662, the PPARγ-specific inhibitor, can repressed the effects of Rg3 on ox-LDL-stimulated HUVECs. For in vivo assay, Rg3 significantly reduced atherosclerotic pathological changes in ApoE^−/− mice fed with HFD, up-regulated PPARγ, and inhibited activation FAK in aorta, thus inhibited expression of VCAM-1, ICAM-1 in intima. We conclude that Rg3 may protect endothelial cells and inhibit atherosclerosis by up-regulating PPARγ via repressing FAK-mediated pathways, indicating that Rg3 have good potential in preventing dyslipidemia induced atherosclerosis.

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Jawi MM, Frohlich J, Chan SY. Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule. J Lipids 2020;2020:3491764. [PMID: 32099678 PMCID: PMC7016456 DOI: 10.1155/2020/3491764] [Citation(s) in RCA: 62] [Impact Index Per Article: 12.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/26/2019] [Accepted: 08/17/2019] [Indexed: 12/15/2022] Open

Ward NC, Kostner KM, Sullivan DR, Nestel P, Watts GF. Molecular, Population, and Clinical Aspects of Lipoprotein(a): A Bridge Too Far? J Clin Med 2019;8:E2073. [PMID: 31783529 PMCID: PMC6947201 DOI: 10.3390/jcm8122073] [Citation(s) in RCA: 13] [Impact Index Per Article: 2.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/29/2019] [Revised: 11/15/2019] [Accepted: 11/15/2019] [Indexed: 12/16/2022] Open

Van den Hof M, Klein Haneveld MJ, Blokhuis C, Scherpbier HJ, Jansen HPG, Kootstra NA, Dallinga-Thie GM, Van Deventer SJH, Tsimikas S, Pajkrt D. Elevated Lipoprotein(a) in Perinatally HIV-Infected Children Compared With Healthy Ethnicity-Matched Controls. Open Forum Infect Dis 2019;6:ofz301. [PMID: 31660394 PMCID: PMC6736182 DOI: 10.1093/ofid/ofz301] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/08/2019] [Indexed: 01/06/2023] Open

Abstract

Background

HIV-associated cardiovascular disease (CVD) risk in combination antiretroviral therapy (cART)-treated perinatally HIV-infected patients (PHIV+) remains unknown due to the young age of this population. Lipoprotein(a) (Lp(a)) has been established as an independent causal risk factor for CVD in the general population but has not been well established in the population of PHIV+.

Methods

We cross-sectionally compared lipid profiles, including nonfasting Lp(a), together with total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides between 35 cART-treated PHIV+ children aged 8-18 years and 37 controls who were matched for age, sex, ethnicity, and socioeconomic status. We explored associations between Lp(a) and disease- and treatment-related factors (inflammation, monocyte activation, and vascular), biomarkers, and neuroimaging outcomes using linear regression models.

Results

PHIV+ children had significantly higher levels of Lp(a) compared with controls (median, 43.6 [21.6-82.4] vs 21.8 [16.8-46.6] mg/dL; P = .033). Other lipid levels were comparable between groups. Additional assessment of apolipoprotein B, apolipoprotein CIII, apolipoprotein E, and APOE genotype revealed no significant differences. Higher Lp(a) levels were associated with higher plasma apoB levels and with lower monocyte chemoattractant protein-1 and TG levels in PHIV+ children. Lp(a) was not associated with HIV- or cART-related variables or with neuroimaging outcomes.

Conclusions

cART-treated PHIV+ children appear to have higher levels of Lp(a) compared with ethnicity-matched controls, which may implicate higher CVD risk in this population. Future research should focus on the association between Lp(a) and (sub)clinical CVD measurements in cART-treated PHIV+ patients.

Dutch Trial Register number

NRT4074.

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Tada H, Takamura M, Kawashiri MA. Lipoprotein(a) as an Old and New Causal Risk Factor of Atherosclerotic Cardiovascular Disease. J Atheroscler Thromb 2019;26:583-591. [PMID: 31061262 PMCID: PMC6629747 DOI: 10.5551/jat.rv17034] [Citation(s) in RCA: 30] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/11/2018] [Accepted: 04/02/2019] [Indexed: 12/16/2022] Open

Schnitzler JG, Dallinga-Thie GM, Kroon J. The Role of (Modified) Lipoproteins in Vascular Function: A Duet Between Monocytes and the Endothelium. Curr Med Chem 2019;26:1594-1609. [PMID: 29546830 DOI: 10.2174/0929867325666180316121015] [Citation(s) in RCA: 18] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/01/2017] [Revised: 12/05/2017] [Accepted: 12/06/2017] [Indexed: 12/24/2022]

Tuten A, Gungor Z, Ekmekci H, Ekmekci OB, Kucur M, Yilmaz N, Donma O, Sonmez H, Acıkgoz A, Madazlı R. Relationship between LPA SNPs and inflammatory burden in patients with preeclampsia to address future cardiovascular risk. J Matern Fetal Neonatal Med 2019;34:898-906. [PMID: 31113255 DOI: 10.1080/14767058.2019.1622667] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]

Sáez T, de Vos P, Kuipers J, Sobrevia L, Faas MM. Exosomes derived from monocytes and from endothelial cells mediate monocyte and endothelial cell activation under high d-glucose conditions. Immunobiology 2019;224:325-333. [PMID: 30827721 DOI: 10.1016/j.imbio.2019.02.004] [Citation(s) in RCA: 17] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/05/2017] [Revised: 10/04/2018] [Accepted: 02/04/2019] [Indexed: 01/22/2023]

Abstract

Diabetes mellitus type 2 (DMT2) is characterized by hyperglycemia and associated with low grade inflammation affecting both endothelial cells and monocytes. Exosomes are nanovesicles, allow communication between endothelial cells and monocytes and have been associated with diabetic complications. In this study we evaluated whether high glucose can activate monocytes and endothelial cells and whether exosomes play a role in this activation. Moreover, we studied whether endothelial cells and monocytes communicate with each other via exosomes under high and basal glncubation. In the first experiment, monomac 6 cells (MM6) were exposed to high glucose (HG; 25 mmol/L) or to exosomes from MM6 exposed to HG (exoMM6-HG) or basal glucose (5.5 mmol/L) (exoMM6-BG). In the second experiment, MM6 were exposed to exosomes from human umbilical vein endothelial cells (HUVECs) and HUVECs to exosomes from MM6. In the third experiment, MM6 and HUVECs were exposed to a mixture of exosomes from MM6 and HUVECs (exoMix). Cell activation was evaluated by measuring the protein surface expression of intracellular adhesion molecule-1 (ICAM-1) by flow cytometry. HG increased ICAM-1 expression in MM6 and monocytic exosomes from HG or BG shown similar effect in HG and BG MM6 cells. Exosomes from HUVECs increased ICAM-1 expression in MM6 cells, incubated under HG or BG, while also exosomes from MM6 increased ICAM-1 expression in HUVECs incubated under HG or BG. The combination of exosomes from both cell types (exoMixHG or exoMixBG) also increased ICAM-1 expression in both type cells in most conditions. However, the exoMixBG reversed the effect of HG in both MM6 and HUVECs. Our results show that HG activated monocytes and endothelial cells and that exosomes play a role in this HG-induced cell ICAM-1 expression. We hypothesize that during DMT2, exosomes may act as a communication mechanism between monocytes and endothelial cells, inducing and maintaining activating of both cell types in the presence of high glucose.

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Scipione CA, Koschinsky ML, Boffa MB. Lipoprotein(a) in clinical practice: New perspectives from basic and translational science. Crit Rev Clin Lab Sci 2017;55:33-54. [PMID: 29262744 DOI: 10.1080/10408363.2017.1415866] [Citation(s) in RCA: 19] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/24/2022]

Ellis KL, Boffa MB, Sahebkar A, Koschinsky ML, Watts GF. The renaissance of lipoprotein(a): Brave new world for preventive cardiology? Prog Lipid Res 2017;68:57-82. [DOI: 10.1016/j.plipres.2017.09.001] [Citation(s) in RCA: 47] [Impact Index Per Article: 5.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/29/2017] [Revised: 09/01/2017] [Accepted: 09/05/2017] [Indexed: 12/24/2022]

Ferretti G, Bacchetti T, Johnston TP, Banach M, Pirro M, Sahebkar A. Lipoprotein(a): A missing culprit in the management of athero-thrombosis? J Cell Physiol 2017;233:2966-2981. [DOI: 10.1002/jcp.26050] [Citation(s) in RCA: 46] [Impact Index Per Article: 5.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/01/2017] [Accepted: 06/12/2017] [Indexed: 12/24/2022]

Pirro M, Bianconi V, Paciullo F, Mannarino MR, Bagaglia F, Sahebkar A. Lipoprotein(a) and inflammation: A dangerous duet leading to endothelial loss of integrity. Pharmacol Res 2017;119:178-187. [DOI: 10.1016/j.phrs.2017.02.001] [Citation(s) in RCA: 35] [Impact Index Per Article: 4.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/23/2016] [Revised: 01/08/2017] [Accepted: 02/02/2017] [Indexed: 12/15/2022]

Thrombophilic state in young patients with acute myocardial infarction. J Thromb Thrombolysis 2016;39:474-80. [PMID: 25589366 DOI: 10.1007/s11239-014-1166-2] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 10/24/2022]

Scipione CA, Sayegh SE, Romagnuolo R, Tsimikas S, Marcovina SM, Boffa MB, Koschinsky ML. Mechanistic insights into Lp(a)-induced IL-8 expression: a role for oxidized phospholipid modification of apo(a). J Lipid Res 2015;56:2273-85. [PMID: 26474593 DOI: 10.1194/jlr.m060210] [Citation(s) in RCA: 82] [Impact Index Per Article: 8.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/27/2015] [Indexed: 12/14/2022] Open

Kassimatis TI, Goldsmith DJA. Statins in chronic kidney disease and kidney transplantation. Pharmacol Res 2014;88:62-73. [PMID: 24995940 DOI: 10.1016/j.phrs.2014.06.011] [Citation(s) in RCA: 19] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/11/2014] [Revised: 06/18/2014] [Accepted: 06/19/2014] [Indexed: 12/15/2022]

Hesperidin inhibits inflammatory response induced by Aeromonas hydrophila infection and alters CD4+/CD8+ T cell ratio. Mediators Inflamm 2014;2014:393217. [PMID: 24891765 PMCID: PMC4033591 DOI: 10.1155/2014/393217] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/21/2013] [Accepted: 03/21/2014] [Indexed: 12/26/2022] Open

Assessment of plasma prothrombotic factors in patients with Buerger's disease. Blood Coagul Fibrinolysis 2013;24:133-9. [PMID: 23358197 DOI: 10.1097/mbc.0b013e32835b7272] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/26/2022]

Abstract

The pathogenesis of Buerger' disease (thrombangiitis obliterans; TAO) remains unknown, although a strong association with tobacco use has been established. Blood coagulation and fibrinolytic factors as well as selected clinical chemistry parameters have been evaluated in 37 patients with Buerger's disease. Median levels of prothrombotic factors were higher in patients with TAO than in healthy control: annexin V (P < 0.0003), factor VII (P < 0.0001), factor VIII (P < 0.0000001), factor XI (P < 0.000003), homocysteine (P < 0.014) and fibrinogen (P = 0.00007). Patients with Buerger's disease also showed higher median plasma levels of urokinase type plasminogen activator (uPA) (P < 0.000004), its receptor (uPAR) (P < 0.0008) and uPA complex with plasminogen activator inhibitor 1 (uPA-PAI-1) P < 0.000006). In contrast, plasma concentrations of apolipoprotein A and folic acid were lower in patients with TAO than in control (P < 0.004 and P < 0.0006; respectively). Higher plasminogen (P < 0.05) and cholesterol (P < 0.003), as well as lower folic acid (P < .0.05) levels were noted in the smokers group than in nonsmoking patients. We found higher plasminogen (P < 0.05), factor VII (P < 0.05), total lipids (P < 0.003), cholesterol (P < 0.05) and triglycerides (P < 0.002) levels in patients requiring surgical treatment for limb-threatening ischaemia than the patients treated only conservatively. These findings suggest an important role of haemostatic risk factors in the pathogenesis of Buerger's disease, with special regard to hyperhomocysteinemia that might be aggravated by low serum folic acid level. In patients with aggressive clinical course, disturbances in serum lipids were more pronounced. Further studies are warranted to establish whether diet supplementation of folic acid as well as normalization of lipids balance might influence the clinical course of TAO.

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Lipoprotein(a) in cardiovascular diseases. BIOMED RESEARCH INTERNATIONAL 2012;2013:650989. [PMID: 23484137 PMCID: PMC3591100 DOI: 10.1155/2013/650989] [Citation(s) in RCA: 46] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 09/06/2012] [Revised: 11/06/2012] [Accepted: 11/08/2012] [Indexed: 11/18/2022]

Lipoprotein(a): Cellular Effects and Molecular Mechanisms. CHOLESTEROL 2012;2012:923289. [PMID: 22991657 PMCID: PMC3443569 DOI: 10.1155/2012/923289] [Citation(s) in RCA: 44] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 06/11/2012] [Accepted: 07/24/2012] [Indexed: 01/31/2023]

McAuley AK, Sanfilippo PG, Connell PP, Wang JJ, Dirani M, Lamoureux E, Hewitt AW. Circulating biomarkers of diabetic retinopathy: a systematic review and meta-analysis. ACTA ACUST UNITED AC 2012. [DOI: 10.2217/dmt.12.4] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/21/2022]

Balogh E, Bereczky Z, Katona E, Koszegi Z, Edes I, Muszbek L, Czuriga I. Interaction between homocysteine and lipoprotein(a) increases the prevalence of coronary artery disease/myocardial infarction in women: a case-control study. Thromb Res 2011;129:133-8. [PMID: 21803402 DOI: 10.1016/j.thromres.2011.07.001] [Citation(s) in RCA: 18] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/23/2010] [Revised: 06/29/2011] [Accepted: 07/05/2011] [Indexed: 11/18/2022]

Gaeta G, Lanero S, Barra S, Silvestri N, Cuomo V, Materazzi C, Vitagliano G. Sex hormones and lipoprotein(a) concentration. Expert Opin Investig Drugs 2011;20:221-38. [DOI: 10.1517/13543784.2011.548804] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/05/2022]

Shin SK, Kwon JH, Jeong YJ, Jeon SM, Choi JY, Choi MS. Supplementation of cheonggukjang and red ginseng cheonggukjang can improve plasma lipid profile and fasting blood glucose concentration in subjects with impaired fasting glucose. J Med Food 2010;14:108-13. [PMID: 21128827 DOI: 10.1089/jmf.2009.1366] [Citation(s) in RCA: 27] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/13/2022] Open

Nakagami F, Nakagami H, Osako MK, Iwabayashi M, Taniyama Y, Doi T, Shimizu H, Shimamura M, Rakugi H, Morishita R. Estrogen attenuates vascular remodeling in Lp(a) transgenic mice. Atherosclerosis 2010;211:41-7. [DOI: 10.1016/j.atherosclerosis.2010.01.016] [Citation(s) in RCA: 20] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/10/2009] [Revised: 01/12/2010] [Accepted: 01/13/2010] [Indexed: 11/25/2022]

The role of lipoprotein-associated phospholipase A2 in atherosclerosis may depend on its lipoprotein carrier in plasma. Biochim Biophys Acta Mol Cell Biol Lipids 2009;1791:327-38. [PMID: 19272461 DOI: 10.1016/j.bbalip.2009.02.015] [Citation(s) in RCA: 117] [Impact Index Per Article: 7.3] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/23/2008] [Revised: 02/06/2009] [Accepted: 02/19/2009] [Indexed: 01/28/2023]

Abstract

Platelet-activating factor (PAF) acetylhydrolase exhibits a Ca(2+)-independent phospholipase A2 activity and degrades PAFas well as oxidized phospholipids (oxPL). Such phospholipids are accumulated in the artery wall and may play key roles in vascular inflammation and atherosclerosis. PAF-acetylhydrolase in plasma is complexed to lipoproteins; thus it is also referred to as lipoprotein-associated phospholipase A2 (Lp-PLA2). Lp-PLA2 is primarily associated with low-density lipoprotein (LDL), whereas a small proportion of circulating enzyme activity is also associated with high-density lipoprotein (HDL). The majority of the LDL-associated Lp-PLA2 (LDL-Lp-PLA2) activity is bound to atherogenic small-dense LDL particles and it is a potential marker of these particles in plasma. The distribution of Lp-PLA2 between LDL and HDL is altered in various types of dyslipidemias. It can be also influenced by the presence of lipoprotein (a) [Lp(a)] when plasma levels of this lipoprotein exceed 30 mg/dl. Several lines of evidence suggest that the role of plasma Lp-PLA2 in atherosclerosis may depend on the type of lipoprotein particle with which this enzyme is associated. In this regard, data from large Caucasian population studies have shown an independent association between the plasma Lp-PLA2 levels (which are mainly influenced by the levels of LDL-Lp-PLA2) and the risk of future cardiovascular events. On the contrary, several lines of evidence suggest that HDL-associated Lp-PLA2 may substantially contribute to the HDL antiatherogenic activities. Recent studies have provided evidence that oxPL are preferentially sequestered on Lp(a) thus subjected to degradation by the Lp(a)-associated Lp-PLA2. These data suggest that Lp(a) may be a potential scavenger of oxPL and provide new insights into the functional role of Lp(a) and the Lp(a)-associated Lp-PLA2 in normal physiology as well as in inflammation and atherosclerosis. The present review is focused on recent advances concerning the Lp-PLA2 structural characteristics, the molecular basis of the enzyme association with distinct lipoprotein subspecies, as well as the potential role of Lp-PLA2 associated with different lipoprotein classes in atherosclerosis and cardiovascular disease.

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