Thioredoxin protects mitochondrial structure, function and biogenesis in myocardial ischemia-reperfusion via redox-dependent activation of AKT-CREB- PGC1α pathway in aged mice
Jaganathan Subramani, Venkatesh Kundumani‐Sridharan, Kumuda C. Das
Abstract
mice resulted in decreased PGC1α expression that decreased mitochondrial gene expression with increased myocardial apoptosis. High levels of Trx, but not mitochondrial thioredoxin (Trx-2) maintained Trx redox balance in I/R resulting in increased PGC1α expression via AKT/CREB activation upregulating mitochondrial gene expression and protection against I/R injury.
Topics & Concepts
ThioredoxinMitochondrial biogenesisMFN2CardioprotectionMitochondrionProtein kinase BReperfusion injuryApoptosisChemistryCREBMitochondrial ROSThioredoxin reductaseInternal medicineEndocrinologyBiologyIschemiaCell biologyMedicineOxidative stressBiochemistryMitochondrial DNAmitochondrial fusionGeneTranscription factorRedox biology and oxidative stressElectron Spin Resonance StudiesSulfur Compounds in Biology