Exosome-Mediated Rewiring of Oxidative Stress-Inflammation-ECM Remodeling Axis Mitigates UVB-Triggered Skin Photoaging

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Photoaging is a chronic and multifactorial form of skin aging primarily induced by ultraviolet (UV) radiation. It is characterized by oxidative stress, DNA damage, chronic inflammation, pigmentary alterations, and extracellular matrix (ECM) degradation, which ultimately lead to wrinkle formation, loss of elasticity, and uneven pigmentation. Exosomes, nanosized extracellular vesicles that mediate intercellular communication, have attracted growing attention in photoaging research. Emerging evidence suggests that exosomes may both contribute to photoaging and promote tissue repair by modulating cellular responses. However, despite the growing body of evidence, the field still lacks an integrated review that links exosome biogenesis and functional properties to the mechanisms of photoaging, their therapeutic potential, and the major translational barriers to clinical application. Therefore, this review aims to systematically summarize the biogenesis and biological properties of exosomes, clarify their mechanistic roles in photoaging, particularly in the regulation of oxidative stress, and evaluate their potential as therapeutic agents and delivery platforms for anti-photoaging and regenerative medicine. It further examines the effects of native exosomes derived from multiple cell sources, with a focus on stem cells, keratinocytes, and melanocytes. Finally, it outlines translationa

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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