NO in turn increased HIF‐1α and VEGF expression that dose‐dependently stimulated chronic ischemic vascular remodeling.[70] In a heart failure model, H2S therapy resulted in cardioprotection by activating the eNOS‐NO‐cGMP and Akt‐VEGF pathways in addition to preserving mitochondrial function to comprehensively enhance angiogenesis and temper oxidative stress.[71]. Here, VEGFA is linked to heart failure.