Mitochondrial ROS

[7][8] Finally, high levels of mitochondrial ROS activate apoptosis/autophagy pathways capable of inducing cell death.

The infection triggers mitochondrial ROS production, which induces stabilization of hypoxia-inducible factor-1α (HIF1A) and consequently promotes glycolysis.

Targeting mitochondrial ROS may have great therapeutic potential for the development of novel drugs to treat patients with coronavirus.

Epidermal cells in mutant mice with a genetic SOD2 deficiency undergo cellular senescence, nuclear DNA damage, and irreversible arrest of proliferation in a portion of their keratinocytes.

[13] This aging phenotype includes weight loss, skin atrophy, kyphosis (curvature of the spine), osteoporosis, muscle degeneration and reduced life span.