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In renal disorders, excessive mitochondrial ROS together with ROS derived from NOX enzymes intensify mitochondrial injury and dissipate the organelles membrane potential (40, 41)

Lupus autoantibodies initiate neuroinflammation sustained by continuous HMGB1:RAGE signaling and reversed by increased LAIR-1 expression

The genomic and epigenomic integrity of gametes further raises the stakes: even subthreshold ROS-induced lesions may result in fertilization failure, impaired embryo development, or transgenerational genomic instability (43, 4648)

Dermatologists and anti-aging doctors are cautiously optimistic

doi: 10.1002/mas.20207