Endothelial / cardiovascular

Empagliflozin improved endothelial vasorelaxation and reduced inflammatory/oxidative stress in human HFpEF myocardium via restored NO-sGC-cGMP-PKG signaling, and the SGLT2i class carries guideline-level cardiovascular outcome benefit.

In the SELECT RCT (17,604 patients with established CVD, overweight/obesity, no diabetes), weekly subcutaneous semaglutide 2.4 mg reduced major adverse cardiovascular events by 20% vs placebo (HR 0.80, 95% CI 0.72-0.90).

In porcine metabolic syndrome, the mitochondria-targeted peptide elamipretide preserved coronary endothelial-cell mitochondria, restored eNOS and endothelium-dependent relaxation, and reduced subendocardial microvascular loss.

Humanin prevented high-glucose-induced endothelial dysfunction in human endothelial cells by inducing KLF2, restoring eNOS and reducing VCAM-1/E-selectin and monocyte adhesion; direct human outcome evidence is still lacking.

MOTS-c, a mitochondria-derived peptide, modulates AMPK, mTOR and sirtuin signaling in endothelial and vascular smooth-muscle cells and is proposed as a therapeutic and biomarker candidate to mitigate endothelial dysfunction and vascular aging.

In men with benign prostatic hyperplasia, tadalafil 5 mg daily significantly improved vascular endothelial function (reactive hyperemia index) and reduced arterial stiffness (brachial-ankle pulse-wave velocity).