Research Perspective Volume 4, Issue 2 pp 116—118

Figure 1. Scheme illustrating the putative role of SOD2 in skin aging.

(Left panel) In normal mice, SOD2 scavenges superoxide anions O₂⁻, a byproduct of mitochondrial respiration, resulting in normal levels of reactive oxygen species (ROS, red stars). This homeostasis leads to minimal cellular stress (little damage to DNA, lipids and proteins), resulting in normal skin, characterized by a thin stratum corneum (SC) and a thick epidermis (EP). (Right panel) In contrast, SOD2 deficiency leads to elevated levels of ROS and oxidative stress (increased damage to DNA, proteins and lipids) as well as impaired mitochondrial (complex II) activity. This results in premature aging, characterized by increased thickness of the stratum corneum (SC) and thinning of the epidermis (EP). The change of the stratum corneum is accompanied by the accumulation of differentiated keratinocytes with high levels of β-galactosidase activity, while the thinning epidermis results from a combination of decreased proliferation and increased senescence in the suprabasal layer (yellow). Compared to normal mice, SOD2 KO mice exhibit elevated skin transcript levels of Tgm1 and p16INK4a, markers for differentiated keratinocytes and cellular senescence respectively, as well as decreased transcript levels for keratin 1(krt1) and keratin 10 (krt10), two markers of transit amplifying cells and early differentiating cells.