ArticleFrontiers in pharmacology2026
ClC-3 mediates angiotensin II-induced endothelial dysfunction by inhibiting Akt-Hsp90-eNOS signaling pathway.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Empagliflozin Improves Endothelial Function in an Ovariectomized Rat Model of Estrogen Deficiency.Journal of cardiovascular translational research · 2026Article
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7 authors.
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Abstract
Background: Endothelial dysfunction is a major driver for hypertension and diabetes. Chloride (Cl Methods: This study aims to explore the role and mechanism of ClC-3 in endothelial dysfunction during hypertension, by using primary cultured human umbilical vein endothelial cells (HUVECs) and ClC-3 knockout mice. Results: We found that AngiotensinII (AngII) treatment significantly upregulated ClC-3 expression and reduced NO levels, while ClC-3 interference increased eNOS phosphorylation. Furthermore, in AngII-infused hypertensive mouse models, ClC-3 knockout significantly increased the phosphorylation level of eNOS and improved vascular relaxation function. Discussion: Our findings suggest that ClC-3 may serve as an important target for hypertension-related endothelial dysfunction, potentially providing new strategies and interventions for the treatment of hypertension and its complications.
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