Abstract
Photoaged skin features an appearance of premature aging induced by external factors, mainly ultraviolet (UV) irradiation. Visible aging signs and increased susceptibility to skin-related diseases triggered by UV irradiation have raised widespread concern. As a critical component of human skin, the extracellular matrix (ECM) provides essential structural, mechanical, and functional support to the tissue. Consequently, UV-induced ECM deterioration is a major contributor to photoaging. This review begins by analyzing the structural and functional changes between healthy and photoaged skin in prominent ECM components, including collagens, glycosaminoglycans (GAGs), proteoglycans, basement membrane proteins, and elastic fibers. Furthermore, we explore the key mechanisms driving ECM deterioration in response to UV irradiation, focusing on mitogen-activated protein kinase/matrix metalloproteinase and transforming growth factor-β/Smad signaling pathways, as well as the synthesis and degradation of GAGs. A comprehensive understanding of these changes and underlying mechanisms is crucial for elucidating the biological influence of UV on the ECM, ultimately providing more reliable evidence for the prevention and treatment of skin photoaging.
Impact Statement
The extracellular matrix (ECM), a fundamental component of the skin, experiences substantial changes after exposure to chronic ultraviolet (UV) irradiation, leading to the deterioration of the skin’s structure, function, and appearance. In addition to investigating the structural and functional differences in the ECM between healthy and photoaged skin, including collagen, glycosaminoglycans, proteoglycans, basement membrane proteins, and elastic fiber, this review analyses the mechanisms by which UV irradiation induces these changes. By targeting different molecules implicated in these cellular processes, it becomes feasible to rejuvenate the skin and augment its resistance to diseases.
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