MIF Family Cytokines as Common Mediators of UV-Induced Photocarcinogenesis and Photoaging

Abstract Ultraviolet (UV) radiation is a major environmental factor responsible for photocarcinogenesis and photoaging. Although these conditions have traditionally been regarded as distinct consequences of chronic UV exposure, accumulating evidence suggests that they share common molecular mechanisms mediated by macrophage migration inhibitory factor (MIF) family cytokines. MIF and its homolog D-dopachrome tautomerase (D-DT, also known as MIF-2) have emerged as important regulators of UV-induced skin damage. MIF family cytokines promote photocarcinogenesis by enhancing inflammatory responses and suppressing apoptosis of UV-damaged keratinocytes. They also contribute to photoaging by regulating matrix metalloproteinase expression, collagen degradation, and extracellular matrix remodeling. Together, these findings indicate that MIF family cytokines coordinate inflammation and tissue remodeling underlying both photocarcinogenesis and photoaging, highlighting them as promising therapeutic targets for preventing chronic UV-induced skin damage.