ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Mineralocorticoid receptor antagonism attenuates experimental pulmonary hypertension.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.
- Pooled it
- Effectiveness of spironolactone plus ambrisentan for treatment of pulmonary arterial hypertension (from the [ARIES] study 1 and 2 trials).The American journal of cardiology · 2013Trial
- Repurposing Heart Failure Therapies in Pulmonary Arterial Hypertension: Mechanistic Rationale, Translational Evidence, and Clinical Perspectives for SGLT2 Inhibitors and Mineralocorticoid Receptor Antagonists.Medicina (Kaunas, Lithuania) · 2026Review
- Why we need treatment? Prognosis of tricuspid regurgitation.European heart journal supplements : journal of the European Society of Cardiology · 2026Article
- Interplay between medical and interventional therapies in valvular heart disease and heart failure: an expert opinion paper.ESC heart failure · 2026Review
- Management of Tricuspid Valve Regurgitation Consensus Recommendations.Heart views : the official journal of the Gulf Heart Association · 2026Review
- Right Ventricular Fibrosis With Pulmonary Arterial Hypertension.Reviews in cardiovascular medicine · 2025Review
- Mineralocorticoid receptor activation contributes to intestinal fibrosis through neutrophil gelatinase-associated lipocalin in preclinical models.Nature communications · 2025Article
- Pulmonary Hypertension Associated with Interstitial Lung Disease (PH-ILD): Back to the Future.Advances in therapy · 2025Review
- Efficacy of spironolactone in pulmonary arterial hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2025Article
- Eplerenone, a mineralocorticoid receptor inhibitor, reduces cirrhosis associated changes of hepatocyte glucose and lipid metabolism.Cell communication and signaling : CCS · 2024Article
- Mineralocorticoid Receptors in Vascular Smooth Muscle: Blood Pressure and Beyond.Hypertension (Dallas, Tex. : 1979) · 2024Review
- The novel molecular mechanism of pulmonary fibrosis: insight into lipid metabolism from reanalysis of single-cell RNA-seq databases.Lipids in health and disease · 2024Review
- More than just a small left ventricle: the right ventricular fibroblast and ECM in health and disease.American journal of physiology. Heart and circulatory physiology · 2023Review
- The influence of steroid type on outcomes in patients with acute respiratory distress syndrome.Journal of intensive care · 2023Article
- New Drugs and Therapies in Pulmonary Arterial Hypertension.International journal of molecular sciences · 2023Review
- Emerging vascular cell-specific roles for mineralocorticoid receptor: implications for understanding sex differences in cardiovascular disease.American journal of physiology. Cell physiology · 2023Review
- Therapeutic targeting of mineralocorticoid receptors in pulmonary hypertension: Insights from basic research.Frontiers in cardiovascular medicine · 2023Review
- Pannexin 1: a novel regulator of acute hypoxic pulmonary vasoconstriction.Cardiovascular research · 2022Article
- The Platelet-Derived Growth Factor Pathway in Pulmonary Arterial Hypertension: Still an Interesting Target?Life (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Mineralocorticoid receptor (MR) activation stimulates systemic vascular and left ventricular remodeling. We hypothesized that MR contributes to pulmonary vascular and right ventricular (RV) remodeling of pulmonary hypertension (PH). We evaluated the efficacy of MR antagonism by spironolactone in two experimental PH models; mouse chronic hypoxia-induced PH (prevention model) and rat monocrotaline-induced PH (prevention and treatment models). Last, the biological function of the MR was analyzed in cultured distal pulmonary artery smooth muscle cells (PASMCs). In hypoxic PH mice, spironolactone attenuated the increase in RV systolic pressure, pulmonary arterial muscularization, and RV fibrosis. In rat monocrotaline-induced PH (prevention arm), spironolactone attenuated pulmonary vascular resistance and pulmonary vascular remodeling. In the established disease (treatment arm), spironolactone decreased RV systolic pressure and pulmonary vascular resistance with no significant effect on histological measures of pulmonary vascular remodeling, or RV fibrosis. Spironolactone decreased RV cardiomyocyte size modestly with no significant effect on RV mass, systemic blood pressure, cardiac output, or body weight, suggesting a predominantly local pulmonary vascular effect. In distal PASMCs, MR was expressed and localized diffusely. Treatment with the MR agonist aldosterone, hypoxia, or platelet-derived growth factor promoted MR translocation to the nucleus, activated MR transcriptional function, and stimulated PASMC proliferation, while spironolactone blocked these effects. In summary, MR is active in distal PASMCs, and its antagonism prevents PASMC proliferation and attenuates experimental PH. These data suggest that MR is involved in the pathogenesis of PH via effects on PASMCs and that MR antagonism may represent a novel therapeutic target for this disease.
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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.