• Adrenal gland hyperplasia
• Chrousos syndrome
• Glucocorticoid receptor
• Hypertension
• Soluble epoxide hydrolase

• Animals
• Rats
• Hypertension/metabolism
• Hypertension/genetics
• Receptors, Glucocorticoid/metabolism
• Receptors, Glucocorticoid/genetics
• Male
• Sodium Chloride, Dietary
• Fatty Acids, Unsaturated/metabolism
• Fatty Acids, Unsaturated/blood
• Aorta/metabolism
• Blood Pressure
• Mutation
• Epoxide Hydrolases/genetics
• Epoxide Hydrolases/metabolism

• N-403-07-23 National Center of Competence in Research
• 31003A-182478/1 Swiss National Science Foundation grants
• 310030-214978 Swiss National Science Foundation grants
• University of Lausanne

• Cardiovascular disease
• Endothelial cells
• Glucocorticoid resistance
• Glucocorticoids
• Inflammation
• Major depressive disorder

• Humans
• Cardiovascular Diseases/etiology
• Glucocorticoids
• Inflammation/immunology
• Animals
• Signal Transduction
• Endothelial Cells/metabolism
• Depression/immunology
• Depression/physiopathology
• Endothelium, Vascular/physiopathology
• Receptors, Glucocorticoid/metabolism
• Hypothalamo-Hypophyseal System/metabolism
• Pituitary-Adrenal System/metabolism
• Depressive Disorder, Major/immunology

• T32GM007518 NIH HHS
• T32GM007518 NIH HHS
• R01MH123093 NIH HHS
• URECA Stony Brook University

• Case report
• Hypertension
• Infants
• Pharmacogenomics
• Preterm

Hypertension is one of the leading causes of premature death in humans and exhibits a complex aetiology including environmental and genetic factors. Mutations within the glucocorticoid receptor (GR) can cause glucocorticoid resistance, which is characterized by several clinical features like hypercortisolism, hypokalaemia, adrenal hyperplasia and hypertension. Altered glucocorticoid receptor signalling further affects sodium and potassium homeostasis as well as blood pressure regulation and cell proliferation and differentiation that influence organ development and function. In salt-sensitive hypertension, excessive renal salt transport and sympathetic nervous system stimulation may occur simultaneously, and, thus, both the mineralocorticoid receptor (MR) and the GR-signalling may be implicated or even act interdependently. This review focuses on identified GR mutations in human primary generalized glucocorticoid resistance (PGGR) patients and their related clinical phenotype with specific emphasis on adrenal gland hyperplasia and hypertension. We compare these findings to mouse and rat mutants harbouring genetically engineered mutations to further dissect the cause and/or the consequence of clinical features which are common or different.

• Animal model
• Epithelial transport
• Glucocorticoid resistance
• Homeostasis
• Hypercortisolism
• Kidney physiology

• YAP
• diabetic retinopathy
• endothelial cells
• extracellular matrix
• glucocorticoids

Glucocorticoids, as multifunctional hormones, are widely used in the treatment of various diseases including nephrological disorders. They are known to affect immunological cells, effectively treating many autoimmune and inflammatory processes. Furthermore, there is a growing body of evidence demonstrating the potent role of glucocorticoids in non-immune cells such as podocytes. Moreover, novel data show additional pathways and processes affected by glucocorticoids, such as the Wnt pathway or autophagy. The endothelium is currently considered as a key organ in the regulation of numerous kidney functions such as glomerular filtration, vascular tone and the regulation of inflammation and coagulation. In this review, we analyse the literature concerning the effects of endothelial glucocorticoid receptor signalling on kidney function in health and disease, with special focus on hypertension, diabetic kidney disease, glomerulopathies and chronic kidney disease. Recent studies demonstrate the potential role of endothelial GR in the prevention of fibrosis of kidney tissue and cell metabolism through Wnt pathways, which could have a protective effect against disease progression. Another important aspect covered in this review is blood pressure regulation though GR and eNOS. We also briefly cover potential therapies that might affect the endothelial glucocorticoid receptor and its possible clinical implications, with special interest in selective or local GR stimulation and potential mitigation of GC treatment side effects.

• diabetic kidney disease
• endothelium
• glomerulopathy
• glucocorticoid receptor
• glucocorticoids
• kidney

Glucocorticoids (GCs) have been the mainstay of immunosuppressive therapy in solid organ transplantation (SOT) for decades, due to their potent effects on innate immunity and tissue protective effects. However, some SOT centers are reluctant to administer GCs long-term because of the various related side effects. This review summarizes the advantages and disadvantages of GCs in SOT. PubMed and Scopus databases were searched from 2011 to April 2021 using search syntaxes covering “transplantation” and “glucocorticoids”. GCs are used in transplant recipients, transplant donors, and organ perfusate solution to improve transplant outcomes. In SOT recipients, GCs are administered as induction and maintenance immunosuppressive therapy. GCs are also the cornerstone to treat acute antibody- and T-cell-mediated rejections. Addition of GCs to organ perfusate solution and pretreatment of transplant donors with GCs are recommended by some guidelines and protocols, to reduce ischemia-reperfusion injury peri-transplant. GCs with low bioavailability and high potency for GC receptors, such as budesonide, nanoparticle-mediated targeted delivery of GCs to specific organs, and combination use of dexamethasone with inducers of immune-regulatory cells, are new methods of GC application in SOT patients to reduce side effects or induce immune-tolerance instead of immunosuppression. Various side effects involving different non-targeted organs/tissues, such as bone, cardiovascular, neuromuscular, skin and gastrointestinal tract, have been noted for GCs. There are also potential drug-drug interactions for GCs in SOT patients.

• Corticosteroids
• Glucocorticoids
• Solid organ transplantation
• Liver
• Kidney
• Heart
• Lung

• amyloid precursor protein
• hypercortisolism
• pulse-wave velocity
• stress hormone
• α-adrenergic receptor-dependent contraction

• Adrenergic alpha-1 Receptor Agonists/pharmacology
• Alzheimer Disease/blood
• Alzheimer Disease/genetics
• Alzheimer Disease/physiopathology
• Amyloid beta-Protein Precursor/genetics
• Amyloid beta-Protein Precursor/metabolism
• Animals
• Aorta, Thoracic/drug effects
• Aorta, Thoracic/metabolism
• Aorta, Thoracic/physiopathology
• Arterial Pressure
• Corticosterone/blood
• Disease Models, Animal
• Male
• Mice, Inbred C57BL
• Mice, Transgenic
• Mutation
• Receptors, Adrenergic, alpha-1/metabolism
• Up-Regulation
• Vascular Stiffness
• Vasoconstriction/drug effects
• Mice

In the context of the coronavirus disease 2019 (COVID-19) pandemic, the global healthcare community has raced to find effective therapeutic agents against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). To date, dexamethasone is the first and an important therapeutic to significantly reduce the risk of death in COVID-19 patients with severe disease. Due to powerful anti-inflammatory and immunosuppressive effects, dexamethasone could attenuate SARS-CoV-2-induced uncontrolled cytokine storm, severe acute respiratory distress syndrome and lung injury. Nevertheless, dexamethasone treatment is a double-edged sword, as numerous studies have revealed that it has significant adverse impacts later in life. In this article, we reviewed the literature regarding the adverse effects of dexamethasone administration on different organ systems as well as related disease pathogenesis in an attempt to clarify the potential harms that may arise in COVID-19 patients receiving dexamethasone treatment. Overall, taking the threat of COVID­19 pandemic into account, we think it is necessary to apply dexamethasone as a pharmaceutical therapy in critical patients. However, its adverse side effects cannot be ignored. Our review will help medical professionals in the prognosis and follow-up of patients treated with dexamethasone. In addition, given that a considerable amount of uncertainty, confusion and even controversy still exist, further studies and more clinical trials are urgently needed to improve our understanding of the parameters and the effects of dexamethasone on patients with SARS-CoV-2 infection.

• COVID-19
• Depression
• Dexamethasone
• Diabetes
• Necrosis of the femoral head
• Patients
• SARS-CoV-2

The glucocorticoid receptor (GR) is a member of the nuclear receptor family that controls key biological processes in the cardiovascular system and has recently been shown to modulate Wnt signaling in endothelial cells. Wnt/β-catenin signaling has been demonstrated to be crucial in the process of angiogenesis. In the current study, we studied whether GR could regulate angiogenesis via the Wnt/β-catenin pathway.

Key components of the Wnt/β-catenin pathway were evaluated using quantitative PCR and Western blot in the presence or absence of GR. Enhanced angiogenesis was found in GR deficiency in vitro and confirmed with cell viability assays, proliferation assays and tube formation assays. Consistent with these in vitro findings, endothelial cell-specific GR loss GR in vivo promoted angiogenesis in both a hind limb ischemia model and sponge implantation assay. Results were further verified in a novel mouse model lacking endothelial LRP5/6, a key receptor in canonical Wnt signaling, and showed substantially suppressed angiogenesis using these same in vitro and in vivo assays. To further investigate the mechanism of GR regulation of Wnt signaling, autophagy flux was investigated in endothelial cells by visualizing auto phagolysosomes as well as by assessing P62 degradation and LC3B conversion. Results indicated that potentiated autophagy flux participated in GR-Wnt regulation.

Lack of endothelial GR triggers autophagy flux, leads to activation of Wnt/β-catenin signaling and promotes angiogenesis. There may also be a synergistic interaction between autophagy and Wnt/β-catenin signaling.

The online version of this article (10.1007/s10456-021-09773-x) contains supplementary material, which is available to authorized users.

• Angiogenesis
• Autophagy
• Endothelium
• Glucocorticoid receptor
• Wnt/β-catenin pathway

• Animals
• Low Density Lipoprotein Receptor-Related Protein-6/genetics
• Low Density Lipoprotein Receptor-Related Protein-6/metabolism
• Mice
• Mice, Knockout
• Neovascularization, Physiologic
• Receptors, Glucocorticoid/deficiency
• Receptors, Glucocorticoid/metabolism
• Up-Regulation
• Wnt Signaling Pathway
• beta Catenin/genetics
• beta Catenin/metabolism

• R01HL107205 NHLBI NIH HHS
• R01 HL131952 NHLBI NIH HHS
• R01 HL144476 NHLBI NIH HHS
• National Heart, Lung, and Blood Institute

• SP-1
• eNOS
• progesterone
• progesterone receptor-A/B
• vascular relaxation

• Animals
• Aorta, Thoracic/drug effects
• Aorta, Thoracic/enzymology
• Binding Sites
• Cell Nucleus/drug effects
• Cell Nucleus/metabolism
• Cells, Cultured
• Enzyme Induction
• Female
• Hormone Antagonists/pharmacology
• Human Umbilical Vein Endothelial Cells/drug effects
• Human Umbilical Vein Endothelial Cells/enzymology
• Humans
• Mesenteric Arteries/drug effects
• Mesenteric Arteries/enzymology
• Nitric Oxide Synthase Type III/biosynthesis
• Nitric Oxide Synthase Type III/genetics
• Progesterone/pharmacology
• Promoter Regions, Genetic
• Rats, Sprague-Dawley
• Receptors, Progesterone/agonists
• Receptors, Progesterone/antagonists & inhibitors
• Receptors, Progesterone/metabolism
• Signal Transduction
• Sp1 Transcription Factor/metabolism
• Vasodilation/drug effects

• Glucocorticoid
• HIF1
• Hypertension
• NADPH oxidase
• Pulmonary vascular remodeling
• ROS
• p22phox

Synthetic glucocorticoids (GCs) are widely used to treat inflammatory conditions. However, chronic use of GCs can lead to hypertension. The cause of this undesired side effect remains unclear. Previously, we developed an in vivo rat model to study the mechanisms underlying hypertension induced by the chronic administration of the potent synthetic GC, dexamethasone (DEX) and found that the catecholamine biosynthetic pathway plays an important role. In the current study, we used this model to investigate the role of the adrenal medulla, renal nerves, and other peripheral sympathetic nerves in DEX-induced hypertension. After 5 days of baseline telemetric recording of mean arterial pressure (MAP) and heart rate (HR), rats were subjected to one of the following treatments: renal denervation (RDNX), adrenal medullectomy (ADMX), 6-hydroxydopamine (6-OHDA, 20 mg/kg, i.p.) to induce chemical sympathectomy, or a combination of ADMX and 6-OHDA. On day 11, the animals received vehicle (VEH) or DEX in drinking water for 7 days, with the latter causing an increase in MAP in control animals. ADMX and RDNX by themselves exacerbated the pressor effect of DEX. In the chemical sympathectomy group, DEX still caused a rise in MAP but the response was lower (ΔMAP of 6-OHDA/DEX < VEH/DEX, p = 0.039). However, when ΔMAP was normalized to day 10, 6-OHDA + DEX did not show any difference from VEH + DEX, certainly not an increase as observed in DEX + ADMX or RDNX groups. This indicates that sympathetic nerves do not modulate the pressor effect of DEX. TH mRNA levels increased in the adrenal medulla in both VEH/DEX (p = 0.009) and 6-OHDA/DEX (p = 0.031) groups. In the 6-OHDA group, DEX also increased plasma levels of norepinephrine (NE) (p = 0.016). Our results suggest that the activation of catecholamine synthetic pathway could be involved in the pressor response to DEX in animals even under chemical sympathectomy with 6-OHDA.

• 6-OHDA
• adrenal medulla
• dexamethasone
• hypertension
• renal denervation
• sympathetic nerves

The glucocorticoid receptor is a member of the nuclear receptor family that controls many distinct gene networks, governing various aspects of development, metabolism, inflammation, and the stress response, as well as other key biological processes in the cardiovascular system. Recently, research in both animal models and humans has begun to unravel the profound complexity of glucocorticoid signaling and convincingly demonstrates that the glucocorticoid receptor has direct effects on the heart and vessels in vivo and in vitro. This research has contributed directly to improving therapeutic strategies in human disease. The glucocorticoid receptor is activated either by the endogenous steroid hormone cortisol or by exogenous glucocorticoids and acts within the cardiovascular system via both genomic and non-genomic pathways. Polymorphisms of the glucocorticoid receptor are also reported to influence the progress and prognosis of cardiovascular disease. In this review, we provide an update on glucocorticoid signaling and highlight the critical role of this signaling in both physiological and pathological conditions of the cardiovascular system. With increasing in-depth understanding of glucocorticoid signaling, the future is promising for the development of targeted glucocorticoid treatments and improved clinical outcomes.

• blood pressure
• cardiovascular disease
• circadian rhythm
• glucocorticoid receptor
• heart failure
• nuclear hormone
• sepsis

• Animals
• Cardiovascular Diseases/genetics
• Cardiovascular Diseases/metabolism
• Cardiovascular System/metabolism
• Gene Expression Regulation
• Humans
• Hydrocortisone/metabolism
• Polymorphism, Genetic
• Prognosis
• Receptors, Glucocorticoid/genetics
• Receptors, Glucocorticoid/metabolism
• Signal Transduction

• R01 HL131952 NHLBI NIH HHS

Rosiglitazone (RGZ), a peroxisome proliferator-activated receptor gamma (PPARγ) ligand, has been reported to act as insulin sensitizer and exert cardiovascular actions. In this work, we hypothesized that RGZ exerts a PPARγ–dependent regulation of blood pressure through modulation of angiotensin-converting enzyme (ACE)-type 2 (ACE2)/angiotensin-(1-7)/angiotensin II type-2 receptor (AT₂R) axis in an experimental model of high blood pressure. We carried on experiments in normotensive (Sham) and aortic coarctation (AoCo)-induced hypertensive male Wistar rats. Both sham and AoCo rats were treated 7 days with vehicle (V), RGZ (5 mg/kg/day), or RGZ+BADGE (120 mg/kg/day) post-coarctation. We measured blood pressure and vascular reactivity on aortic rings, as well as the expression of renin-angiotensin system (RAS) proteins. We found that RGZ treatment in AoCo group decreases blood pressure values and improves vascular response to acetylcholine, both parameters dependent on PPARγ-stimulation. RGZ lowered serum angiotensin II (AngII) but increased Ang-(1-7) levels. It also decreased 8-hydroxy-2′-deoxyguanosine (8-OH-2dG), malondialdehyde (MDA), and improved the antioxidant capacity. Regarding protein expression of RAS, RGZ decreases ACE and angiotensin II type 1 receptor (AT₁R) and improved ACE2, AT₂R, and Mas receptor in AoCo rats. Additionally, an in silico analysis revealed that 5′UTR regions of RAS and PPARγ share motifs with a transcriptional regulatory role. We conclude that RGZ lowers blood pressure values by increasing the expression of RAS axis proteins ACE2 and AT₂R, decreasing the levels of AngII and increasing levels of Ang-(1-7) in a PPARγ-dependent manner. The in silico analysis is a valuable tool to predict the interaction between PPARγ and RAS.

• Mendelian forms of hypertension
• angiogenesis
• argininosuccinate lyase
• argininosuccinic aciduria
• endothelial cells
• endothelial dysfunction
• hypertension
• induced pluripotent stem cells
• nitric oxide
• oxidative stress

Salt-sensitive hypertension is common in glucocorticoid excess. Glucocorticoid resistance also presents with hypercortisolemia and hypertension but the relationship between salt intake and blood pressure (BP) is not well defined. GR^βgeo/+ mice have global glucocorticoid receptor (GR) haploinsufficiency and increased BP. Here we examined the effect of high salt diet on BP, salt excretion and renal blood flow in GR^βgeo/+mice. Basal BP was ∼10 mmHg higher in male GR^βgeo/+ mice than in GR^+/+ littermates. This modest increase was amplified by ∼10 mmHg following a high-salt diet in GR^βgeo/+ mice. High salt reduced urinary aldosterone excretion but increased renal mineralocorticoid receptor expression in both genotypes. Corticosterone, and to a lesser extent deoxycorticosterone, excretion was increased in GR^βgeo/+ mice following a high-salt challenge, consistent with enhanced 24 h production. GR^+/+ mice increased fractional sodium excretion and reduced renal vascular resistance during the high salt challenge, retaining neutral sodium balance. In contrast, sodium excretion and renal vascular resistance did not adapt to high salt in GR^βgeo/+ mice, resulting in transient sodium retention and sustained hypertension. With high-salt diet, Slc12a3 and Scnn1a mRNAs were higher in GR^βgeo/+ than controls, and this was reflected in an exaggerated natriuretic response to thiazide and benzamil, inhibitors of NCC and ENaC, respectively. Reduction in GR expression causes salt-sensitivity and an adaptive failure of the renal vasculature and tubule, most likely reflecting sustained mineralocorticoid receptor activation. This provides a mechanistic basis to understand the hypertension associated with loss-of-function polymorphisms in GR in the context of habitually high salt intake.

• ENaC
• aldosterone
• hypertension
• mineralocorticoid
• renal
• sodium
• steroids
• thiazide

• Animals
• Glucocorticoids/metabolism
• Humans
• Mice, Knockout
• Organ Specificity
• Receptors, Glucocorticoid/agonists
• Receptors, Glucocorticoid/genetics
• Receptors, Glucocorticoid/metabolism
• Signal Transduction

• R00 ES022983 NIEHS NIH HHS
• R01 HD087288 NICHD NIH HHS

The metabolic syndrome describes a clustering of risk factors—visceral obesity, dyslipidaemia, insulin resistance, and salt-sensitive hypertension—that increases mortality related to cardiovascular disease, type 2 diabetes, cancer, and non-alcoholic fatty liver disease. The prevalence of these concurrent comorbidities is ~ 25–30% worldwide, and metabolic syndrome therefore presents a significant global public health burden. Evidence from clinical and preclinical studies indicates that glucocorticoid excess is a key causal feature of metabolic syndrome. This is not increased systemic in circulating cortisol, rather increased bioavailability of active glucocorticoids within tissues. This review examines the role of covert glucocorticoid excess on the hypertension of the metabolic syndrome. Here, the role of the 11β-hydroxysteroid dehydrogenase enzymes, which exert intracrine and paracrine control over glucocorticoid signalling, is examined. 11βHSD1 amplifies glucocorticoid action in cells and contributes to hypertension through direct and indirect effects on the kidney and vasculature. The deactivation of glucocorticoid by 11βHSD2 controls ligand access to glucocorticoid and mineralocorticoid receptors: loss of function promotes salt retention and hypertension. As for hypertension in general, high blood pressure in the metabolic syndrome reflects a complex interaction between multiple systems. The clear association between high dietary salt, glucocorticoid production, and metabolic disorders has major relevance for human health and warrants systematic evaluation.

• 11β-Hydroxysteroid dehydrogenases
• Aldosterone
• Cortisol
• Glucocorticoid excess
• Hypertension
• Metabolic syndrome
• Salt retention
• Salt-sensitivity

Nephrotic syndrome is a common disorder in adults and children whose etiology is largely unknown. Glucocorticoids remain the mainstay of therapy in most cases, though their mechanism of action remains poorly understood. Emerging evidence suggests that immunomodulatory therapies used in nephrotic syndrome directly target the podocytes. To study how steroids directly affect the podocytes in the treatment of proteinuria, we created a mouse model with podocyte-specific deletion of the glucocorticoid receptor. The podocyte-specific glucocorticoid receptor (GR) knockout mice had similar renal function and protein excretion compared to wild type. However, after glomerular injury induced by either LPS or nephrotoxic serum, the podocyte GR knockout mice demonstrated worsened proteinuria compared to wild type. Ultrastructural examination of podocytes confirmed more robust foot process effacement in the knockout animals. Expression of several key slit diaphragm protein was down regulated in pGR KO mice. Primary podocytes isolated from wild type and podocyte GR knockout mice showed similar actin stress fiber staining patterns in unstimulated conditions. Yet, when exposed to LPS, GR knockout podocytes demonstrated fewer stress fibers and impaired migration compared to wild type podocytes. We conclude that the podocyte glucocorticoid receptor is important for limiting proteinuria in settings of podocyte injury.

• Number of relapses
• Número de recaídas
• Remission time
• Steroid toxicity
• Steroid-sensitive nephrotic syndrome
• Síndrome nefrótico cortico-sensible
• Tiempo de remisión
• Toxicidad esteroide

• Developmental programming
• Glucocorticoid
• Hypertension
• Melatonin
• Melatonin receptor
• Nuclear receptor

• Animals
• Blood Pressure/drug effects
• Dexamethasone/adverse effects
• Female
• Gene Expression Regulation/drug effects
• Heart/drug effects
• Hypertension/chemically induced
• Hypertension/metabolism
• Hypertension/pathology
• Hypertension/physiopathology
• Kidney/drug effects
• Kidney/metabolism
• Male
• Melatonin/metabolism
• Melatonin/pharmacology
• Mothers
• Pregnancy
• Prenatal Exposure Delayed Effects/chemically induced
• Prenatal Exposure Delayed Effects/metabolism
• Prenatal Exposure Delayed Effects/pathology
• Prenatal Exposure Delayed Effects/physiopathology
• Rats
• Rats, Sprague-Dawley
• Receptors, Melatonin/genetics
• Receptors, Melatonin/metabolism
• Signal Transduction/drug effects

• atherosclerosis
• endothelium
• glucocorticoid receptor

• Aluminum Hydroxide/adverse effects
• Angiostrongylus cantonensis/chemistry
• Animals
• Asthma/drug therapy
• Asthma/genetics
• Asthma/immunology
• Asthma/pathology
• Bronchoalveolar Lavage Fluid/immunology
• Cystatins/administration & dosage
• Cystatins/immunology
• Cytokines/biosynthesis
• Eosinophils/immunology
• Helminth Proteins/administration & dosage
• Helminth Proteins/immunology
• Humans
• Immunologic Factors/administration & dosage
• Immunologic Factors/immunology
• Interferon-gamma/genetics
• Interferon-gamma/immunology
• Interleukin-10/genetics
• Interleukin-10/immunology
• Interleukin-17/genetics
• Interleukin-17/immunology
• Interleukin-4/genetics
• Interleukin-4/immunology
• Interleukin-5/genetics
• Interleukin-5/immunology
• Interleukin-6/genetics
• Interleukin-6/immunology
• Male
• Neutrophils/immunology
• Ovalbumin/adverse effects
• Rats
• Rats, Wistar

• Animals
• Anti-Inflammatory Agents/pharmacology
• Dexamethasone/pharmacology
• Endothelium/drug effects
• Endothelium/metabolism
• Glucocorticoids/metabolism
• Interleukin-6/metabolism
• Lipopolysaccharides/pharmacology
• Male
• Mice
• NF-kappa B/metabolism
• Nitric Oxide/metabolism
• Receptors, Glucocorticoid/metabolism
• Sepsis/drug therapy
• Sepsis/metabolism
• Tumor Necrosis Factor-alpha/metabolism

• HL61371 NHLBI NIH HHS
• HL64793 NHLBI NIH HHS
• P30 DK079310 NIDDK NIH HHS
• U24 DK59635 NIDDK NIH HHS
• R01 HL064793 NHLBI NIH HHS
• K08-DK078623 NIDDK NIH HHS
• R37 HL061371 NHLBI NIH HHS
• R01 HL096670 NHLBI NIH HHS
• K08 DK078623 NIDDK NIH HHS
• R01 HL081190 NHLBI NIH HHS
• R01 HL061371 NHLBI NIH HHS
• HL096670 NHLBI NIH HHS
• P01 HL107205 NHLBI NIH HHS
• HL081190 NHLBI NIH HHS
• U24 DK059635 NIDDK NIH HHS

• Carrier
• Drug
• Glucocorticoids

• Animals
• Atherosclerosis/metabolism
• Atherosclerosis/pathology
• Humans
• Orphan Nuclear Receptors/physiology
• Receptors, Calcitriol/physiology
• Receptors, Retinoic Acid/physiology
• Receptors, Steroid/physiology
• Signal Transduction

• Pediatric endocrine hypertension
• adrenal
• aldosterone
• essential hypertension