ArticleYonago acta medica2014
Glucocorticoids Induce Cardiac Fibrosis via Mineralocorticoid Receptor in Oxidative Stress: Contribution of Elongation Factor Eleven-Nineteen Lysine-Rich Leukemia (ELL).
Article in Yonago acta medica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- Glucocorticoid resistance-induced inflammation drives cardiovascular-kidney-metabolic (CKM) syndrome pathophysiology.Trends in endocrinology and metabolism: TEM · 2026Review
- Cardiac response to chronic restraint stress involves mineralocorticoid receptors in male Sprague-Dawley rats.Physiological reports · 2025Article
- [Dilated cardiomyopathy in a patient with Cushing's disease - clinical presentation, diagnosis and treatment: a case report].Problemy endokrinologii · 2025Article
- Cardiac Endocrine Function and Hormonal Interplay in Pediatrics: From Development to Clinical Implications.Biomedicines · 2025Review
- The Role of Chronic Stress in the Pathogenesis of Ischemic Heart Disease in Women.Comprehensive Physiology · 2025Review
- Importance of Micromilieu for Pathophysiologic Mineralocorticoid Receptor Activity-When the Mineralocorticoid Receptor Resides in the Wrong Neighborhood.International journal of molecular sciences · 2022Review
- Psychosocial Stress Hastens Disease Progression and Sudden Death in Mice with Arrhythmogenic Cardiomyopathy.Journal of clinical medicine · 2020Article
- Glucocorticoids and programming of the microenvironment in heart.The Journal of endocrinology · 2019Review
- Pharmacological Treatment of Heart Failure with Preserved Ejection Fraction.Yonago acta medica · 2017Review
- Beneficial effects of mineralocorticoid receptor blockade in experimental non-alcoholic steatohepatitis.Liver international : official journal of the International Association for the Study of the Liver · 2015Article
- Eplerenone attenuates cardiac dysfunction and oxidative stress in β-receptor stimulated myocardial infarcted rats.American journal of translational research · 2015Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCardiac fibrosis is considered to be a crucial factor in the development of heart failure. Blockade of the mineralocorticoid receptor (MR) attenuated cardiac fibrosis and improved the prognosis of patients with chronic heart failure but the ligand for MR and the regulatory mechanism of MR pathway in the diseased heart are unclear. Here, we investigated whether glucocorticoids can promote cardiac fibrosis through MR in oxidative stress and the involvement of elongation factor eleven-nineteen lysine-rich leukemia (ELL), a co-activator of MR, in this pathway. METHODS AND
resultsThe MR antagonist eplerenone attenuated corticosterone-induced collagen synthesis assessed by [(3)H]proline incorporation in rat neonatal cultured cardiac fibroblasts in the presence of H2O2, as an oxidative stress but not in the absence of H2O2. H2O2 increased the ELL expression levels and MR-bound ELL. ELL expression levels and MR-bound ELL were also increased in the left ventricle of heart failure model rats with significant fibrosis and enhanced oxidative stress. Eplerenone did not attenuate corticosterone-induced increase of [(3)H]proline incorporation in the presence of H2O2 after knockdown of ELL expression using small interfering RNA in cardiac fibroblasts.
conclusionGlucocorticoids can promote cardiac fibrosis via MR in oxidative stress, and oxidative stress modulates MR response to glucocorticoids through the interaction with ELL. Preventing cardiac fibrosis by modulating glucocorticoid-MR-ELL pathway may become a new therapeutic strategy for heart failure.
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Identifiers
25349466PMC4209341W2171278730What OpenQuestion holds
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.