<scp>FM</scp>19<scp>G</scp>11 reverses endothelial dysfunction in rat and human arteries through stimulation of the <scp>PI3K/Akt/eNOS</scp> pathway, independently of <scp>mTOR</scp>/<scp>HIF</scp>‐1α activation

Abstract

Stimulation of the PI3K/Akt/eNOS pathway by FM19G11 alleviates impaired NO-mediated endothelial vasodilatation in rat and human arteries independently of mTOR/HIF-1α activation. This pharmacological strategy could be beneficial for managing pathological conditions associated with endothelial dysfunction, such as ED.