Mitochondrial dysfunction in metabolic syndrome and inflammatory skin disease

Metabolic syndrome is a multifactorial process characterized by obesity, hypertension, hyperlipidemia, hyperglycemia, and insulin resistance, significantly increasing the risk of cardiovascular disease (CVD), type 2 diabetes mellitus, and other chronic health conditions. The prevalence of metabolic syndrome is rising globally due to sedentary lifestyles and poor dietary habits. Inflammatory skin diseases, including psoriasis, atopic dermatitis (AD), rosacea, acne vulgaris, lichen planus, acanthosis nigricans, androgenetic alopecia and hidradenitis suppurativa are closely linked to metabolic syndrome and mitochondrial dysfunction. These skin conditions are characterized by dysregulated immune responses and increased activation of inflammatory cytokines and immune cells. Additionally, mechanisms resulting in the induction of mitochondrial apoptosis influence the pathogenesis of these inflammatory skin diseases, while oxidative stress, inflammation and insulin resistance further interlink mitochondrial dysfunction and metabolic syndrome. Understanding the role of mitochondrial dysfunction in the pathogenesis of metabolic syndrome and inflammatory skin diseases is crucial for developing targeted therapies. Further research is needed to explore the contributing pathophysiology and develop strategies for preventing and treating these conditions. Genomic studies have also identified mutations associated with mitochondrial dysfunction and insulin resistance, offering potential targets for personalized therapies. Key words: Mitochondrial dysfunction, Metabolic syndrome, Insulin resistance, Autoinflammatory skin disease, Oxidative stress