ArticleSexual medicine2026
Angiotensin (1-7) improves diabetes mellitus-induced erectile dysfunction in rats by modulating the Cav-1/eNOS signaling pathway.
Article in Sexual medicine, 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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Abstract
Introduction: Diabetes mellitus-induced erectile dysfunction (DMED) is a common complication of diabetes and is often associated with impaired nitric oxide (NO) signaling and increased oxidative stress. Angiotensin (1-7) (Ang (1-7)) has been reported to exert protective effects in cardiovascular and metabolic disorders; however, its role and underlying mechanisms in DMED remain incompletely understood. This study investigated whether Ang (1-7) improves erectile function in DMED through regulation of the caveolin-1 (Cav-1)/endothelial nitric oxide synthase (eNOS) signaling pathway. Methods: A type 2 diabetes mellitus rat model was established and divided into control, diabetes mellitus (DM), DMED, DMED treated with Ang (1-7), and DMED treated with saline groups. Erectile function was evaluated by the intracavernous pressure to mean arterial pressure ratio (ICP/MAP). Cav-1, eNOS, and phosphorylated eNOS (p-eNOS Ser1177) expression in corpus cavernosum tissue was assessed by western blot. Plasma NO and peroxynitrite (ONOO Results: DMED rats exhibited reduced erectile function, decreased Cav-1 expression, reduced eNOS phosphorylation, lower NO levels, and increased ONOO Discussion: Ang (1-7) improves erectile function in DMED rats and protects CCSMCs from high glucose-induced injury. These effects are associated with the restoration of Cav-1/eNOS signaling, enhanced NO bioavailability, reduced oxidative stress, and improved calcium homeostasis. The findings support an important role for caveolae-mediated signaling in DMED and suggest that Ang (1-7) may represent a potential therapeutic strategy for diabetic erectile dysfunction.
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