ArticleScientific reports2015
Aldosterone induces clonal β-cell failure through glucocorticoid receptor.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Targeting the aldosterone-mineralocorticoid receptor pathway in cardiovascular-kidney-metabolic syndrome.Nature reviews. Nephrology · 2026Review
- Aldosterone fuels the progression of cardiovascular-kidney -metabolic syndrome: focus on primary aldosteronism spectrum.Endocrine · 2026Review
- Genetic evidence for the causal relationship between metabolic diseases and primary aldosteronism: insights from Mendelian randomization analysis.Cardiovascular endocrinology & metabolism · 2026Article
- Aldosterone induced by chronic stress promotes pancreatic steatosis in young male rats.Cell and tissue research · 2026Article
- NR3C1/Glucocorticoid receptor activation promotes pancreatic β-cell autophagy overload in response to glucolipotoxicity.Autophagy · 2023Article
- The role of aldosterone and ideal cardiovascular health in incident diabetes: The Jackson Heart Study.American journal of preventive cardiology · 2023Article
- Primary hyperaldosteronism is associated with increased mortality and morbidity in patients with hypertension and diabetes.Frontiers in endocrinology · 2023Article
- Mineralocorticoid Receptor-Associated Mechanisms in Diabetic Kidney Disease and Clinical Significance of Mineralocorticoid Receptor Antagonists.American journal of nephrology · 2023Review
- Role of the Transcription Factor MAFA in the Maintenance of Pancreatic β-Cells.International journal of molecular sciences · 2022Review
- MafA Regulation in β-Cells: From Transcriptional to Post-Translational Mechanisms.Biomolecules · 2022Review
- The mineralocorticoid receptor-an emerging player in metabolic syndrome?Journal of human hypertension · 2021Review
- Comparison of Clinical Features between Primary Aldosteronism and Essential Hypertension in Chinese Patients: A Case-Control Study.International journal of endocrinology · 2021Article
- Effects of Primary Aldosteronism and Different Therapeutic Modalities on Glucose Metabolism.Journal of clinical medicine · 2019Article
- Both aldosterone and spironolactone can modulate the intracellular ACE/ANG II/AT1 and ACE2/ANG (1-7)/MAS receptor axes in human mesangial cells.Physiological reports · 2019Article
- Glucose regulates MafA transcription factor abundance and insulin gene expression by inhibiting AMP-activated protein kinase in pancreatic β-cells.The Journal of biological chemistry · 2018Article
- Primary aldosteronism patients show skin alterations and abnormal activation of glucocorticoid receptor in keratinocytes.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aldosterone excess causes insulin resistance in peripheral tissues and directly impairs the function of clonal β-cell. The aim of this study was to investigate the molecular mechanisms involved in the aldosterone-induced impairment of clonal β-cells. As expected, aldosterone induced apoptosis and β-cell dysfunction, including impairment of insulin synthesis and secretion, which were reversed by Glucocorticoid receptor (GR) antagonists or GR-specific siRNA. However, mineralocorticoid receptor (MR) antagonists or MR-specific siRNA had no effect on impairment of clonal β-cells induced by aldosterone. Besides, aldosterone significantly decreased expression and activity of MafA, while activated JNK and p38 MAPK in a GR-dependent manner. In addition, JNK inhibitors (SP600125) and/or p38 inhibitors (SB203580) could abolish the effect of aldosterone on MafA expression and activity. Importantly, overexpression of JNK1 or p38 reversed the protective effect of a GR antagonist on the decrease of MafA expression and activity. Furthermore, aldosterone inhibits MafA expression at the transcriptional and post-transcriptional level through activation of JNK and p38, respectively. Consequently, overexpression of MafA increased synthesis and secretion of insulin, and decreased apoptosis in clonal β-cells exposed to aldosterone. These findings identified aldosterone as an inducer of clonal β-cell failure that operates through the GR-MAPK-MafA signaling pathway.
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