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1
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Progressive development of melanoma-induced cachexia differentially impacts organ systems in mice. Cell Rep 2023; 42:111934. [PMID: 36640353 PMCID: PMC9983329 DOI: 10.1016/j.celrep.2022.111934] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/08/2022] [Revised: 10/12/2022] [Accepted: 12/15/2022] [Indexed: 12/30/2022] Open
Abstract
Cachexia is a systemic wasting syndrome that increases cancer-associated mortality. How cachexia progressively and differentially impacts distinct tissues is largely unknown. Here, we find that the heart and skeletal muscle undergo wasting at early stages and are the tissues transcriptionally most impacted by cachexia. We also identify general and organ-specific transcriptional changes that indicate functional derangement by cachexia even in tissues that do not undergo wasting, such as the brain. Secreted factors constitute a top category of cancer-regulated genes in host tissues, and these changes include upregulation of the angiotensin-converting enzyme (ACE). ACE inhibition with the drug lisinopril improves muscle force and partially impedes cachexia-induced transcriptional changes, although wasting is not prevented, suggesting that cancer-induced host-secreted factors can regulate tissue function during cachexia. Altogether, by defining prevalent and temporal and tissue-specific responses to cachexia, this resource highlights biomarkers and possible targets for general and tissue-tailored anti-cachexia therapies.
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2
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Ausoni S, Calamelli S, Saccà S, Azzarello G. How progressive cancer endangers the heart: an intriguing and underestimated problem. Cancer Metastasis Rev 2021; 39:535-552. [PMID: 32152913 DOI: 10.1007/s10555-020-09869-8] [Citation(s) in RCA: 13] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/07/2023]
Abstract
Since it came into being as a discipline, cardio-oncology has focused on the prevention and treatment of cardiotoxicity induced by antitumor chemotherapy and radiotherapy. Over time, it has been proved that even more detrimental is the direct effect generated by cancer cells that release pro-cachectic factors in the bloodstream. Secreted molecules target different organs at a distance, including the heart. Inflammatory and neuronal modulators released by the tumor bulk, either as free molecules or through exosomes, contribute to the pathogenesis of cardiac disease. Progressive cancer causes cachexia and severe cardiac muscle wasting accompanied by cardiomyocyte atrophy, tissue fibrosis, and several functional impairments up to heart failure. The molecular mechanisms responsible for such a cardiac muscle wasting have been partially elucidated in animal models, but minimally investigated in humans, although severe cardiac dysfunction exacerbates global cachexia and hampers efficient anti-cancer treatments. This review provides an overview of cancer-induced structural cardiac and functional damage, drawing on both clinical and scientific research. We start by looking at the pathophysiological mechanisms and evolving epidemiology and go on to discuss prevention, diagnosis, and a multimodal policy of intervention aimed at providing overall prognosis and global care for patients. Despite much interest in the cardiotoxicity of cancer therapies, the direct tumor effect on the heart remains poorly explored. There is still a lack of diagnostic criteria for the identification of the early stages of cardiac disease in cancer patients, while the possibilities that there are for effective prevention are largely underestimated. Research on innovative therapies has claimed considerable advances in preclinical studies, but none of the molecular targets suitable for clinical application has been approved for therapy. These issues are critically discussed here.
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Affiliation(s)
- Simonetta Ausoni
- Department of Biomedical Sciences, University of Padua, Padova, Italy.
| | - Sara Calamelli
- Department of Cardiology, Local Health Unit 3 Serenissima, Mirano Hospital, Mirano, Venice, Italy
| | - Salvatore Saccà
- Department of Cardiology, Local Health Unit 3 Serenissima, Mirano Hospital, Mirano, Venice, Italy
| | - Giuseppe Azzarello
- Department of Medical Oncology, Local Health Unit 3 Serenissima, Mirano Hospital, Mirano, Venice, Italy.
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3
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Beyond the boundaries of cardiology: Still untapped anticancer properties of the cardiovascular system-related drugs. Pharmacol Res 2019; 147:104326. [DOI: 10.1016/j.phrs.2019.104326] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/24/2019] [Revised: 06/18/2019] [Accepted: 06/21/2019] [Indexed: 02/07/2023]
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4
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Argilés JM, López-Soriano FJ, Stemmler B, Busquets S. Therapeutic strategies against cancer cachexia. Eur J Transl Myol 2019; 29:7960. [PMID: 31019661 PMCID: PMC6460215 DOI: 10.4081/ejtm.2019.7960] [Citation(s) in RCA: 43] [Impact Index Per Article: 7.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/30/2018] [Accepted: 12/18/2018] [Indexed: 01/06/2023] Open
Abstract
Cancer cachexia has two main components: anorexia and metabolic alterations. The main changes associated with the development of this multi-organic syndrome are glucose intolerance, fat depletion and muscle protein hypercatabolism. The aim of this paper is to review the more recent therapeutic approaches designed to counteract the wasting suffered by the cancer patient with cachexia. Among the most promising approaches we can include the use of ghrelin agonists, beta-blockers, beta-adrenergic agonists, androgen receptor agonists and anti-myostatin peptides. The multi-targeted approach seems essential in these treatments, which should include the combination of both nutritional support, drugs and a suitable program of physical exercise, in order to ameliorate both anorexia and the metabolic changes associated with cachexia. In addition, another very important and crucial aspect to be taken into consideration in the design of clinical trials for the treatment of cancer cachexia is to staging cancer patients in relation with the degree of cachexia, in order to start as early as possible this triple approach in the course of the disease, even before the weight loss can be detected.
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Affiliation(s)
- Josep M Argilés
- Cancer Research Group, Department of Biochemistry and Molecular Biomedicine, Biology Faculty of the Barcelona University, Barcelona, Spain.,Biomedicine Institute, Barcelona University (IBUB), Barcelona, Spain
| | - Francisco Javier López-Soriano
- Cancer Research Group, Department of Biochemistry and Molecular Biomedicine, Biology Faculty of the Barcelona University, Barcelona, Spain.,Biomedicine Institute, Barcelona University (IBUB), Barcelona, Spain
| | | | - Sílvia Busquets
- Cancer Research Group, Department of Biochemistry and Molecular Biomedicine, Biology Faculty of the Barcelona University, Barcelona, Spain.,Biomedicine Institute, Barcelona University (IBUB), Barcelona, Spain
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5
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Novel targeted therapies for cancer cachexia. Biochem J 2017; 474:2663-2678. [PMID: 28751550 DOI: 10.1042/bcj20170032] [Citation(s) in RCA: 48] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/13/2017] [Revised: 06/21/2017] [Accepted: 06/23/2017] [Indexed: 02/06/2023]
Abstract
Anorexia and metabolic alterations are the main components of the cachectic syndrome. Glucose intolerance, fat depletion, muscle protein catabolism and other alterations are involved in the development of cancer cachexia, a multi-organ syndrome. Nutritional approach strategies are not satisfactory in reversing the cachectic syndrome. The aim of the present review is to deal with the recent therapeutic targeted approaches that have been designed to fight and counteract wasting in cancer patients. Indeed, some promising targeted therapeutic approaches include ghrelin agonists, selective androgen receptor agonists, β-blockers and antimyostatin peptides. However, a multi-targeted approach seems absolutely essential to treat patients affected by cancer cachexia. This approach should not only involve combinations of drugs but also nutrition and an adequate program of physical exercise, factors that may lead to a synergy, essential to overcome the syndrome. This may efficiently reverse the metabolic changes described above and, at the same time, ameliorate the anorexia. Defining this therapeutic combination of drugs/nutrients/exercise is an exciting project that will stimulate many scientific efforts. Other aspects that will, no doubt, be very important for successful treatment of cancer wasting will be an optimized design of future clinical trials, together with a protocol for staging cancer patients in relation to their degree of cachexia. This will permit that nutritional/metabolic/pharmacological support can be started early in the course of the disease, before severe weight loss occurs. Indeed, timing is crucial and has to be taken very seriously when applying the therapeutic approach.
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Loncar G, Springer J, Anker M, Doehner W, Lainscak M. Cardiac cachexia: hic et nunc. J Cachexia Sarcopenia Muscle 2016; 7:246-60. [PMID: 27386168 PMCID: PMC4929818 DOI: 10.1002/jcsm.12118] [Citation(s) in RCA: 100] [Impact Index Per Article: 11.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/21/2016] [Accepted: 03/18/2016] [Indexed: 12/12/2022] Open
Abstract
Cardiac cachexia (CC) is the clinical entity at the end of the chronic natural course of heart failure (HF). Despite the efforts, even the most recent definition of cardiac cachexia has been challenged, more precisely, the addition of new criteria on top of obligatory weight loss. The pathophysiology of CC is complex and multifactorial. A better understanding of pathophysiological pathways in body wasting will contribute to establish potentially novel treatment strategies. The complex biochemical network related with CC and HF pathophysiology underlines that a single biomarker cannot reflect all of the features of the disease. Biomarkers that could pick up the changes in body composition before they convey into clinical manifestations of CC would be of great importance. The development of preventive and therapeutic strategies against cachexia, sarcopenia, and wasting disorders is perceived as an urgent need by healthcare professionals. The treatment of body wasting remains an unresolved challenge to this day. As CC is a multifactorial disorder, it is unlikely that any single agent will be completely effective in treating this condition. Among all investigated therapeutic strategies, aerobic exercise training in HF patients is the most proved to counteract skeletal muscle wasting and is recommended by treatment guidelines for HF.
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Affiliation(s)
- Goran Loncar
- Department of Cardiology Clinical Hospital Zvezdara Belgrade Serbia; School of Medicine University of Belgrade Belgrade Serbia
| | - Jochen Springer
- Innovative Clinical Trials, Department of Cardiology and Pneumology University Medical Center Göttingen (UMG) Göttingen Germany
| | - Markus Anker
- Department of Cardiology Charité - Universitätsmedizin Berlin Germany
| | - Wolfram Doehner
- Center for Stroke Research Berlin Charité Universitätsmedizin Berlin Germany
| | - Mitja Lainscak
- Department of Cardiology and Department of Research and Education General Hospital Celje Celje Slovenia; Faculty of Medicine University of Ljubljana Ljubljana Slovenia
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Mueller TC, Bachmann J, Prokopchuk O, Friess H, Martignoni ME. Molecular pathways leading to loss of skeletal muscle mass in cancer cachexia--can findings from animal models be translated to humans? BMC Cancer 2016; 16:75. [PMID: 26856534 PMCID: PMC4746781 DOI: 10.1186/s12885-016-2121-8] [Citation(s) in RCA: 60] [Impact Index Per Article: 6.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/05/2014] [Accepted: 02/03/2016] [Indexed: 02/06/2023] Open
Abstract
Background Cachexia is a multi-factorial, systemic syndrome that especially affects patients with cancer of the gastrointestinal tract, and leads to reduced treatment response, survival and quality of life. The most important clinical feature of cachexia is the excessive wasting of skeletal muscle mass. Currently, an effective treatment is still lacking and the search for therapeutic targets continues. Even though a substantial number of animal studies have contributed to a better understanding of the underlying mechanisms of the loss of skeletal muscle mass, subsequent clinical trials of potential new drugs have not yet yielded any effective treatment for cancer cachexia. Therefore, we questioned to which degree findings from animal studies can be translated to humans in clinical practice and research. Discussion A substantial amount of animal studies on the molecular mechanisms of muscle wasting in cancer cachexia has been conducted in recent years. This extensive review of the literature showed that most of their observations could not be consistently reproduced in studies on human skeletal muscle samples. However, studies on human material are scarce and limited in patient numbers and homogeneity. Therefore, their results have to be interpreted critically. Summary More research is needed on human tissue samples to clarify the signaling pathways that lead to skeletal muscle loss, and to confirm pre-selected drug targets from animal models in clinical trials. In addition, improved diagnostic tools and standardized clinical criteria for cancer cachexia are needed to conduct standardized, randomized controlled trials of potential drug candidates in the future.
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Affiliation(s)
- Tara C Mueller
- Department of Surgery, Klinikum rechts der Isar, Technische Universität München, Ismaninger Strasse 22, D-81675, Munich, Germany.
| | - Jeannine Bachmann
- Department of Surgery, Klinikum rechts der Isar, Technische Universität München, Ismaninger Strasse 22, D-81675, Munich, Germany
| | - Olga Prokopchuk
- Department of Surgery, Klinikum rechts der Isar, Technische Universität München, Ismaninger Strasse 22, D-81675, Munich, Germany
| | - Helmut Friess
- Department of Surgery, Klinikum rechts der Isar, Technische Universität München, Ismaninger Strasse 22, D-81675, Munich, Germany
| | - Marc E Martignoni
- Department of Surgery, Klinikum rechts der Isar, Technische Universität München, Ismaninger Strasse 22, D-81675, Munich, Germany
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DELAFONTAINE PATRICE, YOSHIDA TADASHI. THE RENIN-ANGIOTENSIN SYSTEM AND THE BIOLOGY OF SKELETAL MUSCLE: MECHANISMS OF MUSCLE WASTING IN CHRONIC DISEASE STATES. TRANSACTIONS OF THE AMERICAN CLINICAL AND CLIMATOLOGICAL ASSOCIATION 2016; 127:245-258. [PMID: 28066057 PMCID: PMC5216488] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Subscribe] [Scholar Register] [Indexed: 06/06/2023]
Abstract
Sarcopenia and cachexia are muscle-wasting syndromes associated with aging and with many chronic diseases such as congestive heart failure, diabetes, cancer, chronic obstructive pulmonary disease, and renal failure. While mechanisms are complex, these conditions are often accompanied by elevated angiotensin II (Ang II). We found that Ang II infusion in rodents leads to skeletal muscle wasting via alterations in insulin-like growth factor-1 signaling, increased apoptosis, enhanced muscle protein breakdown via the ubiquitin-proteasome system, and decreased appetite resulting from downregulation of hypothalamic orexigenic neuropeptides orexin and neuropeptide Y. Furthermore, Ang II inhibits skeletal muscle stem cell proliferation, leading to lowered muscle regenerative capacity. Distinct stem cell Ang II receptor subtypes are critical for regulation of muscle regeneration. In ischemic mouse congestive heart failure model skeletal muscle wasting and attenuated muscle regeneration are Ang II dependent. These data suggest that the renin-angiotensin system plays a critical role in mechanisms underlying cachexia in chronic disease states.
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Affiliation(s)
- PATRICE DELAFONTAINE
- Correspondence and reprint requests: Patrice Delafontaine, MD,
Department of Medicine and Medical Pharmacology and Physiology, University of Missouri School of Medicine, One Hospital Drive, CE323, Columbia, Missouri 65212573-884-9260573-884-4808
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Cardiac cachexia: hic et nunc: "hic et nunc" - here and now. Int J Cardiol 2015; 201:e1-12. [PMID: 26545926 DOI: 10.1016/j.ijcard.2015.10.115] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/12/2015] [Accepted: 10/13/2015] [Indexed: 02/07/2023]
Abstract
Cardiac cachexia (CC) is the clinical entity at the end of chronic natural course of heart failure (HF). Despite the efforts, even the most recent definition of cardiac cachexia has been challenged, more precisely the addition of new criteria on top of obligatory weight loss. The pathophysiology of CC is complex and multifactorial. Better understanding of pathophysiological pathways in body wasting will contribute to establish potentially novel treatment strategies. The complex biochemical network related with CC and HF pathophysiology underlines that a single biomarker cannot reflect all of the features of the disease. Biomarkers that could pick-up the changes in body composition before they convey into clinical manifestations of CC would be of great importance. The development of preventive and therapeutic strategies against cachexia, sarcopenia and wasting disorders is perceived as an urgent need by healthcare professionals. The treatment of body wasting remains an unresolved challenge to this day. As CC is a multifactorial disorder, it is unlikely that any single agent will be completely effective in treating this condition. Among all investigated therapeutic strategies, aerobic exercise training in HF patients is the most proved to counteract skeletal muscle wasting and is recommended by treatment guidelines for HF.
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10
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Abstract
Sarcopenia and cachexia are muscle wasting syndromes associated with aging and with many chronic diseases, such as congestive heart failure (CHF), diabetes, cancer, chronic obstructive pulmonary disease and chronic kidney disease (CKD). While mechanisms are complex, these conditions are often accompanied by elevated angiotensin II (Ang II). Patients with advanced CHF or CKD often have increased Ang II levels and cachexia, and angiotensin-converting enzyme inhibitor treatment improves weight loss. It was found that Ang II infusion in rodents leads to skeletal muscle wasting. Ang II increases cytokines and circulating hormones, such as tumor necrosis factor-α, interleukin-6, serum amyloid-A and glucocorticoids, which regulate muscle protein synthesis and degradation. Ang II-induced muscle wasting is caused by alterations in insulin-like growth factor-1 signaling, enhanced muscle protein breakdown via the ubiquitin-proteasome system and decreased appetite resulting from the downregulation of hypothalamic orexigenic neuropeptides, such as Npy and orexin. Ang II also inhibits 5' adenosine monophosphate-activated protein kinase activity and disrupts normal energy balance via the activation of 5' adenosine monophosphate-activated protein kinase phosphatase PP2Cα. Furthermore, Ang II inhibits skeletal muscle stem (satellite) cell proliferation, leading to lowered muscle regenerative capacity. Distinct satellite cell angiotensin receptor subtypes have different effects on different stages of differentiation and are critical for the regulation of muscle regeneration. These data suggest that the renin-angiotensin system plays a critical role in mechanisms underlying cachexia in chronic disease states, and it is a promising target for the treatment of muscle atrophy in patients with diseases such as CHF and CKD.
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Affiliation(s)
- Tadashi Yoshida
- Department of Medicine, University of Missouri-Columbia, Columbia, MO
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Mueller TC, Burmeister MA, Bachmann J, Martignoni ME. Cachexia and pancreatic cancer: Are there treatment options? World J Gastroenterol 2014; 20:9361-9373. [PMID: 25071331 PMCID: PMC4110568 DOI: 10.3748/wjg.v20.i28.9361] [Citation(s) in RCA: 48] [Impact Index Per Article: 4.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/29/2013] [Revised: 01/14/2014] [Accepted: 02/17/2014] [Indexed: 02/06/2023] Open
Abstract
Cachexia is frequently described in patients with pancreatic ductal adenocarcinoma (PDAC) and is associated with reduced survival and quality of life. Unfortunately, the therapeutic options of this multi-factorial and complex syndrome are limited. This is due to the fact that, despite extensive preclinical and clinical research, the underlying pathological mechanisms leading to PDAC-associated cachexia are still not fully understood. Furthermore, there is still a lack of consensus on the definition of cachexia, which complicates the standardization of diagnosis and treatment as well as the analysis of the current literature. In order to provide an efficient therapy for cachexia, an early and reliable diagnosis and consistent monitoring is required, which can be challenging especially in obese patients. Although many substances have been tested in clinical and preclinical settings, so far none of them have been proven to have a long-term effect in ameliorating cancer-associated cachexia. However, recent studies have demonstrated that multidimensional therapeutic modalities are able to alleviate pancreatic cancer-associated cachexia and ultimately improve patients’ outcome. In this current review, we propose a stepwise and pragmatic approach to facilitate and standardize the treatment of cachexia in pancreatic cancer patients. This strategy consists of nutritional, dietary, pharmacological, physical and psychological methods.
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Rosiglitazone and imidapril alone or in combination alleviate muscle and adipose depletion in a murine cancer cachexia model. Tumour Biol 2013; 35:323-32. [DOI: 10.1007/s13277-013-1043-1] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/06/2013] [Accepted: 07/18/2013] [Indexed: 01/09/2023] Open
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Murphy KT, Chee A, Trieu J, Naim T, Lynch GS. Inhibition of the renin-angiotensin system improves physiological outcomes in mice with mild or severe cancer cachexia. Int J Cancer 2013; 133:1234-46. [DOI: 10.1002/ijc.28128] [Citation(s) in RCA: 25] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/20/2012] [Accepted: 02/08/2013] [Indexed: 01/20/2023]
Affiliation(s)
- Kate T. Murphy
- Department of Physiology, Basic and Clinical Myology Laboratory; The University of Melbourne; Victoria; 3010; Australia
| | - Annabel Chee
- Department of Physiology, Basic and Clinical Myology Laboratory; The University of Melbourne; Victoria; 3010; Australia
| | - Jennifer Trieu
- Department of Physiology, Basic and Clinical Myology Laboratory; The University of Melbourne; Victoria; 3010; Australia
| | - Timur Naim
- Department of Physiology, Basic and Clinical Myology Laboratory; The University of Melbourne; Victoria; 3010; Australia
| | - Gordon S. Lynch
- Department of Physiology, Basic and Clinical Myology Laboratory; The University of Melbourne; Victoria; 3010; Australia
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Anker MS, von Haehling S, Springer J, Banach M, Anker SD. Highlights of mechanistic and therapeutic cachexia and sarcopenia research 2010 to 2012 and their relevance for cardiology. Arch Med Sci 2013; 9:166-71. [PMID: 23515589 PMCID: PMC3598129 DOI: 10.5114/aoms.2013.33356] [Citation(s) in RCA: 22] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/03/2012] [Revised: 11/05/2012] [Accepted: 11/06/2012] [Indexed: 02/07/2023] Open
Abstract
Sarcopenia and cachexia are significant medical problems with a high disease-related burden in cardiovascular illness. Muscle wasting and weight loss are very frequent particularly in chronic heart failure and they relate to poor prognosis. Although clinically largely underestimated, the fields of cachexia and sarcopenia are of great relevance to cardiologists. In cachexia and sarcopenia a significant number of research publications related to basic science questions of muscle wasting and lipolysis were published between 2010 and 2012. Recently, the two processes of muscle wasting and lipolysis were found to be closely linked. Treatment research in pre-clinical models involves studies on a number of different therapeutic entities, including ghrelin, selective androgen receptor modulators (SARMs), as well as drugs targeting myostatin or melanocortin-4. In the human setting, studies using enobosarm (a SARM) and anamorelin (ghrelin) are in phase III. The last 3 years have seen significant efforts to define the field using consensus statements. In the future, these definitions should also be considered for guidelines and treatment trials in cardiovascular medicine. The current review aims to summarize important information and development in the fields of muscle wasting, sarcopenia and cachexia, focusing on findings in cardiovascular research, in order for cardiologists to have a better understanding of the progress in this still insufficiently known field.
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Affiliation(s)
- Markus S. Anker
- Center for Clinical and Basic Research, IRCCS San Raffaele, Rome, Italy
| | - Stephan von Haehling
- Applied Cachexia Research, Department of Cardiology, Charité, Campus Virchow-Klinikum, Berlin, Germany
| | - Jochen Springer
- Applied Cachexia Research, Center for Cardiovascular Research, Charité, Campus Mitte, Berlin, Germany
| | - Maciej Banach
- Department of Hypertension, Medical University of Lodz, Poland
| | - Stefan D. Anker
- Center for Clinical and Basic Research, IRCCS San Raffaele, Rome, Italy
- Applied Cachexia Research, Department of Cardiology, Charité, Campus Virchow-Klinikum, Berlin, Germany
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Anker MS, von Haehling S, Springer J, Banach M, Anker SD. Highlights of the mechanistic and therapeutic cachexia and sarcopenia research 2010 to 2012 and their relevance for cardiology. Int J Cardiol 2013; 162:73-6. [DOI: 10.1016/j.ijcard.2012.10.018] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/19/2012] [Accepted: 10/20/2012] [Indexed: 12/25/2022]
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