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<p>Extrinsic skin aging reflects cumulative exposome stressors, dominated by ultraviolet radiation and compounded by pollution and smoking. These inputs converge on oxidative stress, which triggers stress kinases and inflammatory transcriptional programs, elevates matrix metalloproteinases, suppresses collagen-anabolic signaling, and weakens the epidermal barrier. Here, we synthesize natural products that target this cascade and organize them by biological source and chemical scaffold to link structure with mechanisms. We map actions onto two tracks: damage interception by limiting reactive oxygen species (ROS) and stress signaling, including Nrf2-linked defenses and DNA photoprotection, and by restraining activator protein 1 (AP-1), nuclear factor <i>κ</i>B (NF-<i>κ</i>B), and matrix metalloproteinases (MMPs); and repair enhancement <i>via</i> extracellular matrix (ECM) rebuilding and barrier restoration. We appraise evidence from 2D cells to 3D skin, animal UV models, and human studies, highlight dose and formulation pitfalls, and propose combination regimens pairing UV filters with bioactives. Finally, we close with translational priorities in delivery, stability, standardization, photosafety, and endpoint-driven clinical trials for personalized systems-level prevention.</p>

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Natural Product Modulation of Oxidative Stress in the Treatment of Extrinsic Skin Aging: Mechanisms of Action and Future Perspectives

  • 期刊论文

  • 发表日期：

    2026年3月21日

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  • Xiujun Zhang,
  • Jiaxuan Wang,
  • Jingjing Kang,
  • Jingqi Li,
  • Junchen Li,
  • Chenqi Guo,
  • Zhiqiang Hao,
  • Dingbin Liu

摘要

Extrinsic skin aging reflects cumulative exposome stressors, dominated by ultraviolet radiation and compounded by pollution and smoking. These inputs converge on oxidative stress, which triggers stress kinases and inflammatory transcriptional programs, elevates matrix metalloproteinases, suppresses collagen-anabolic signaling, and weakens the epidermal barrier. Here, we synthesize natural products that target this cascade and organize them by biological source and chemical scaffold to link structure with mechanisms. We map actions onto two tracks: damage interception by limiting reactive oxygen species (ROS) and stress signaling, including Nrf2-linked defenses and DNA photoprotection, and by restraining activator protein 1 (AP-1), nuclear factor κB (NF-κB), and matrix metalloproteinases (MMPs); and repair enhancement via extracellular matrix (ECM) rebuilding and barrier restoration. We appraise evidence from 2D cells to 3D skin, animal UV models, and human studies, highlight dose and formulation pitfalls, and propose combination regimens pairing UV filters with bioactives. Finally, we close with translational priorities in delivery, stability, standardization, photosafety, and endpoint-driven clinical trials for personalized systems-level prevention.