Empagliflozin re-establishes AMP/ATP, activating adenosine monophosphate (AMP)-activated protein kinase (AMPK), inducing Drp1S637 phosphorylation and decreasing in Drp1S616 phosphorylation, inducing inhibition of mitochondrial fission, thus improving cardiac microvascular injury in T2D mice [109]; other results evidenced that empagliflozin could prevent and/or improve renal ischemia-reperfusion injury through anti-inflammatory effects and the activation of the AMPK-OPA1 pathway, enhancing mitochondrial fusion [110]. Here, OPA1 is linked to type 2 diabetes mellitus.