Mitochondrial-dependent apoptosis and STAT3 activation induced by oxidative stress in pemphigus vulgaris.

In the context of Pemphigus Vulgaris (PV), an autoimmune skin disorder, our study explores the intricate relationship between dyslipidemia, oxidative stress, and mitochondrial-dependent apoptosis in PV. We investigated lipid profiles in PV patients, revealing significant dyslipidemia marked by elevated cholesterol, triglycerides, and apolipoprotein B, alongside decreased high-density lipoprotein and serum calcium levels. The imbalance was found to augment oxidative stress, evident from increased oxidative stress markers in lesion tissues and serum. Notably, oxidative stress correlated with classic PV biomarkers, anti-DSG1/DSG3 antibodies. Lipid-induced oxidative stress was further confirmed in vitro using HaCaT cells treated with PV patient serum, which led to STAT3 activation and mitochondrial-dependent apoptosis. This apoptosis was characterized by changes in mitochondrial membrane potential and activation of apoptotic proteins, implicating oxidative stress as a key player in PV pathogenesis. Our findings suggest the critical connections between lipid disturbances, oxidative stress, apoptosis, and STAT3 activation in PV, offering potential avenues for novel therapeutic interventions.