NIH R01 · 2025
Coronary Vascular Resilience by Modulation of Mitochondrial ROS in Endothelium
The main objective of this study is to elucidate molecular mechanisms by which coronary endothelial cells (EC) can survive and proliferate in ischemic (low oxygen, low glucose) conditions and help improve cardiac This proposal is based on our recent report that reduction in mitochondrial (mito)-ROS, using EC-specific transgenic overexpression of mito-antioxidant MnSOD (SOD-OE) or using mito-specific antioxidant nanoparticle JP4-039, improves survival and proliferation of coronary EC, and help recover cardiac function in a post-myocardial infarct (MI) animal model. Coronary ECs from SOD-OE demonstrated 50% reduction in mito-ROS (by mito-roGFP), significant increase in mitochondrial complexes…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.