ArticleEndocrinology2011
11β-hydroxysteroid dehydrogenase type 2 deficiency accelerates atherogenesis and causes proinflammatory changes in the endothelium in apoe-/- mice.
Article in Endocrinology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 86 citations in OpenAlex.
- Effect of spironolactone on monocyte subsets in atrial fibrillation: IMPRESS-AF randomised controlled trial.Scientific reports · 2025Trial
- Review
- Molecular Pathways of Endothelial Dysfunction Induced by Chronic Social Stress and Therapeutic Interventions.Journal of cardiovascular translational research · 2025Review
- Aldosterone: Essential for Life but Damaging to the Vascular Endothelium.Biomolecules · 2023Review
- Primary Aldosteronism and Ischemic Heart Disease.Frontiers in cardiovascular medicine · 2022Review
- Glucocorticoids: Fuelling the Fire of Atherosclerosis or Therapeutic Extinguishers?International journal of molecular sciences · 2021Review
- Posttranslational Modifications of the Mineralocorticoid Receptor and Cardiovascular Aging.Frontiers in molecular biosciences · 2021Review
- Novel Insight into Neuroimmune Regulatory Mechanisms and Biomarkers Linking Major Depression and Vascular Diseases: The Dilemma Continues.International journal of molecular sciences · 2020Review
- The endothelial mineralocorticoid receptor: Contributions to sex differences in cardiovascular disease.Pharmacology & therapeutics · 2019Review
- Review
- 11β-Hydroxysteroid dehydrogenases control access of 7β,27-dihydroxycholesterol to retinoid-related orphan receptor γ.Journal of lipid research · 2019Article
- Mineralocorticoid receptor: A hidden culprit for hemodialysis vascular access dysfunction.EBioMedicine · 2019Review
- Prediction of Molecular Mechanisms for LianXia NingXin Formula: A Network Pharmacology Study.Frontiers in physiology · 2018Article
- Clinical, genetic, and structural basis of apparent mineralocorticoid excess due to 11β-hydroxysteroid dehydrogenase type 2 deficiency.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Hepatic and Aortic Arch Expression and Serum Levels of Syndecan-1 in ApoEThe open biochemistry journal · 2017Article
- Low-Dose Mineralocorticoid Receptor Blockade Prevents Western Diet-Induced Arterial Stiffening in Female Mice.Hypertension (Dallas, Tex. : 1979) · 2015Article
- Endothelial glucocorticoid receptor suppresses atherogenesis--brief report.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Mineralocorticoid Receptors in the Pathophysiology of Vascular Inflammation and Atherosclerosis.Frontiers in endocrinology · 2015Review
- Mineralocorticoid receptors in immune cells: emerging role in cardiovascular disease.Steroids · 2014Review
- Smooth muscle cell mineralocorticoid receptors: role in vascular function and contribution to cardiovascular disease.Pflugers Archiv : European journal of physiology · 2013Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Mineralocorticoid receptor (MR) activation is proinflammatory and proatherogenic. Antagonism of MR improves survival in humans with congestive heart failure caused by atherosclerotic disease. In animal models, activation of MR exacerbates atherosclerosis. The enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) prevents inappropriate activation of the MR by inactivating glucocorticoids in mineralocorticoid-target tissues. To determine whether glucocorticoid-mediated activation of MR increases atheromatous plaque formation, we generated Apoe(-/-)/11β-HSD2(-/-) double-knockout (E/b2) mice. On chow diet, E/b2 mice developed atherosclerotic lesions by 3 months of age, whereas Apolipoprotein E (Apoe(-/-)) mice remained lesion free. Brachiocephalic plaques in 3-month-old E/b2 mice showed increased macrophage and lipid content and reduced collagen content compared with similar sized brachiocephalic plaques in 6-month-old Apoe(-/-) mice. Crucially, treatment of E/b2 mice with eplerenone, an MR antagonist, reduced plaque development and macrophage infiltration while increasing collagen and smooth muscle cell content without any effect on systolic blood pressure. In contrast, reduction of systolic blood pressure in E/b2 mice using the epithelial sodium channel blocker amiloride produced a less-profound atheroprotective effect. Vascular cell adhesion molecule 1 expression was increased in the endothelium of E/b2 mice compared with Apoe(-/-) mice. Similarly, aldosterone increased vascular cell adhesion molecule 1 expression in mouse aortic endothelial cells, an effect mimicked by corticosterone only in the presence of an 11β-HSD2 inhibitor. Thus, loss of 11β-HSD2 leads to striking atherogenesis associated with activation of MR, stimulating proinflammatory processes in the endothelium of E/b2 mice.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.