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Mitochondrial calcium overload and oxidative stress during ischemia reperfusion (I/R) injury remains a major obstacle during percutaneous coronary intervention after acute myocardial infarction. It often leads to an increased susceptibility for mitochondria permeability transition pore (mPTP) opening leading to cell death. Mitochondrial calcium overload and ROS have been identified as key triggers to open the mPTP for over 30 years, yet the exact mechanism has remained elusive. Additionally, glycogen synthase kinase 3β; (GSK-3β;) is proposed as one of the key molecules that regulate mitochondrial dysfunction and injury during I/R. Indeed inhibition of GSK-3β has been shown to be required for ischemic pre- and postconditioning. Interestingly inhibition of GSK-3β is detrimental during the ischemic phase but beneficial only during the reperfusion stage of I/R injury.

Specific Aims

  1. Identify the GSK-3β mediated phosphorylation site(s) on CypD
  2. Identify the key mechanism of site-specific phosphorylation of CypD on mPTP regulation in the context of Ischemia Reperfusion Injury

Publication Date



mitochondria, mPTP, GSK3β


Cardiology | Medicine and Health Sciences | Translational Medical Research


Presented at the 2019 National Heart, Lung, and Blood Institute Mitochondrial Biology Symposium

GSK3β-dependent phosphorylation of CypD and regulation of mPTP opening during myocardial infarction