Do Not Overcharge the System or It Will Explode!

Ameliorating Endothelial Mitochondrial Dysfunction Restores Coronary Function via Transient Receptor Potential Vanilloid 1–Mediated Protein Kinase A/Uncoupling Protein 2 Pathway

“…31 Mitochondrial ROS generation highly depends on the MMP. 15 Cheurfa et al 17 reported that increased UCP2 expression is associated with a reduced incidence of coronary artery disease in male patients with type 2 diabetes mellitus. Other studies have found that UCP2 overexpression actually reduces endothelial ROS generation, inflammatory activation, and apoptosis.…”

Recent Advances in Mitochondrial Research

“…Silencing of pro-fission proteins restores mitochondrial networks and diminishes reactive oxygen species (ROS) production while increasing the activation state of nitric oxide (NO) synthase 15 , the latter of which could have a direct role in adaptive mitochondrial dynamics 16 . In healthy endothelium, regulatory proteins such as uncoupling protein 2 (UCP2) appear to be integrated with pro-fission responses to protect endothelial cells from the damaging ROS and p53 activation associated with the fragmented mitochondrial phenotype 17, 18 .…”