ArticleJournal of cardiovascular translational research2026
α7-nAChR Activation is Associated with Attenuation of Cardiac Fibrosis in Ischemic Cardiomyopathy via SIRT3-Dependent Modulation of EndMT.
Article in Journal of cardiovascular translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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7 authors.
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Abstract
To investigate whether α7-nicotinic acetylcholine receptor (α7-nAChR) activation attenuates ischemic cardiomyopathy (ICM) through regulation of endothelial-to-mesenchymal transition (EndMT), and to explore the involvement of Sirtuin-3 (SIRT3) in this process. ICM was induced in rats by coronary ligation for 4 weeks, followed by treatment with PNU-282,987, a selective α7-nAChR agonist, or cardiac-specific SIRT3 knockdown using serotype 9 adeno-associated virus (AAV9). Human umbilical vein endothelial cells (HUVECs) were treated with transforming growth factor-β (TGF-β) and/or PNU-282,987 (10 µM). α7-nAChR activation improved cardiac function, reversed ICM-induced TGF-β upregulation and SIRT3 downregulation, and inhibited EndMT-related changes. These effects were weakened by SIRT3 knockdown. The findings suggest that α7-nAChR activation alleviates ICM and myocardial fibrosis through a SIRT3-dependent mechanism, although direct receptor-level specificity requires further validation.
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