Mitochondrial homeostasis: Exploring their impact on skin disease pathogenesis
Hajar Ahmad Jamil, Norwahidah Abdul Karim
Abstract
Mitochondria play a vital impact in maintaining the well-being of the skin, by regulating key cellular activities and processes in various skin cell types, including keratinocytes, fibroblasts, and melanocytes. Understanding their activity and dysfunction is essential for comprehending the pathophysiology of skin diseases and establishing viable therapeutic approaches. This review synthesizes current knowledge on the role of mitochondria in skin cells and their impact on disease progression. In keratinocytes, mitochondria support differentiation and skin barrier formation. In fibroblasts, they are essential for collagen synthesis and maintaining redox balance. In melanocytes, mitochondria facilitate melanin synthesis and protect against UV-induced oxidative damage. Mitochondrial dysfunction, characterized by generation of reactive oxygen species (ROS), alterations in mitochondrial DNA (mtDNA), and changes in biogenesis and dynamics, has been linked to skin diseases such as psoriasis, atopic dermatitis, and vitiligo. These dysfunctions disrupt cellular energy metabolism and stress responses, compromising skin structure and function. Mitochondria are therefore integral not only to energy production and oxidative stress regulation but also to the overall biosynthetic and protective functions of the skin. Future research should aim to deepen our understanding of mitochondrial dysfunction in skin cells and explore targeted strategies to restore mitochondrial health in skin diseases. • Mitochondria regulate key functions in keratinocytes, fibroblasts, and melanocytes. • Mitochondrial dysfunction contributes to psoriasis, atopic dermatitis, and vitiligo. • Oxidative stress from mitochondria contributes to skin inflammation and damage. • Altered mitochondrial DNA, biogenesis and dynamics impact skin cell health. • Restoring mitochondrial function offers new strategies for skin disease treatment.