ArticleMolecular and cellular endocrinology2018
Estrogen receptor beta maintains expression of KLF15 to prevent cardiac myocyte hypertrophy in female rodents.
Article in Molecular and cellular endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Postnatal maternal care impacts hypothalamicbioRxiv : the preprint server for biology · 2025Article
- 17-beta estradiol prevents cardiac myocyte hypertrophy by regulating mitochondrial E3 ubiquitin ligase 1.Cell death & disease · 2025Article
- Membrane-Initiated Estrogen, Androgen, and Progesterone Receptor Signaling in Health and Disease.Endocrine reviews · 2022Review
- PA and OA induce abnormal glucose metabolism by inhibiting KLF15 in adipocytes.Nutrition & metabolism · 2021Article
- Nutraceutical, Dietary, and Lifestyle Options for Prevention and Treatment of Ventricular Hypertrophy and Heart Failure.International journal of molecular sciences · 2021Review
- Impaired branched chain amino acid oxidation contributes to cardiac insulin resistance in heart failure.Cardiovascular diabetology · 2019Article
- Non-genomic Effects of Estrogen on Cell Homeostasis and Remodeling With Special Focus on Cardiac Ischemia/Reperfusion Injury.Frontiers in endocrinology · 2019Review
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Maintaining a healthy, anti-hypertrophic state in the heart prevents progression to cardiac failure. In humans, angiotensin II (AngII) indirectly and directly stimulates hypertrophy and progression, while estrogens acting through estrogen receptor beta (ERβ) inhibit these AngII actions. The KLF15 transcription factor has been purported to provide anti-hypertrophic action. In cultured neonatal rat cardiomyocytes, we found AngII inhibited KLF1 expression and nuclear localization, substantially prevented by estradiol (E2) or β-LGND2 (β-LGND2), an ERβ agonist. AngII stimulation of transforming growth factor beta expression in the myocytes activated p38α kinase via TAK1 kinase, inhibiting KLF15 expression. All was comparably reduced by E2 or β-LGND2. Knockdown of KLF15 in the myocytes induced myocyte hypertrophy and limited the anti-hypertrophic actions of E2 and β-LGND2. Key aspects were confirmed in an in-vivo model of cardiac hypertrophy. Our findings define additional anti-hypertrophic effects of ERβ supporting testing specific receptor agonists in humans to prevent progression of cardiac disease.
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