SIRT3 a Major Player in Attenuation of Hepatic Ischemia-Reperfusion Injury by Reducing ROS via Its Downstream Mediators: SOD2, CYP-D, and HIF-1<i>α</i>

<div>Increased activity of Sirt3 promotes deacetylation of SOD2. Increased activity of Sirt3 promotes deacetylation of SOD2; this reduces the cellular oxidative stress via ROS scavenging. Sirt3 also stabilizes HIF1<i>α</i>, which activates Sirt3 gene promoter that leads to increased synthesis of Sirt3 mRNA transcripts, and deactivates CYPD and subsequently decreases mPTP opening. All these processes orchestrate to reduce hepatocyte damage. Dihydromyricetin (DHM), ischemic preconditioning (IPC), and Resveratrol (RSV).</div>

Oxidative Medicine and Cellular Longevity

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Figure 1

Figure 1: SIRT3 a Major Player in Attenuation of Hepatic Ischemia-Reperfusion Injury by Reducing ROS via Its Downstream Mediators: SOD2, CYP-D, and HIF-1<i>α</i> 

Figure 1 | SIRT3 a Major Player in Attenuation of Hepatic Ischemia-Reperfusion Injury by Reducing ROS via Its Downstream Mediators: SOD2, CYP-D, and HIF-1α 