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<p>Ultraviolet (UV) irradiation is a major cause of photoaging, driving oxidative stress, inflammation, and extracellular matrix (ECM) degradation. Collagen is central to dermal integrity, yet animal-derived sources pose immunogenic and pathogen risks, while recombinant collagens reported to date often lack the stable triple-helical architecture required for bioactivity. Here, we present a triple-helical recombinant humanized type I collagen (THRCI) that combines native-like conformation with excellent biosafety and regenerative efficacy. THRCI supported fibroblast adhesion, proliferation, migration, and collagen synthesis, while suppressing intracellular reactive oxygen species and pro-inflammatory cytokines. In zebrafish, THRCI reduced oxidative stress and alleviated UV-induced caudal fin atrophy. In a murine model of acute UV photodamage, topical THRCI accelerated epidermal recovery, restored hydration and barrier function, increased dermal density, and promoted collagen fiber remodeling, while downregulating <i>IL-6</i>, <i>IL-1β</i>, <i>MMP-1</i>, and <i>MMP-9</i>. Collectively, these findings indicate that THRCI exhibits effective photodamage-repair properties in our established models and represents a promising animal-free collagen biomaterial for skin regeneration.</p> Graphical Abstract <p></p>

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Triple-helical recombinant humanized type I collagen promotes photodamaged skin repair via ECM remodeling and anti-inflammatory mechanisms

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月1日

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  • Nannan Wei,
  • Yuchen Zhang,
  • Wenjie Huang,
  • Xinyu Tian,
  • Linyan Yao,
  • Jianxi Xiao

摘要

Ultraviolet (UV) irradiation is a major cause of photoaging, driving oxidative stress, inflammation, and extracellular matrix (ECM) degradation. Collagen is central to dermal integrity, yet animal-derived sources pose immunogenic and pathogen risks, while recombinant collagens reported to date often lack the stable triple-helical architecture required for bioactivity. Here, we present a triple-helical recombinant humanized type I collagen (THRCI) that combines native-like conformation with excellent biosafety and regenerative efficacy. THRCI supported fibroblast adhesion, proliferation, migration, and collagen synthesis, while suppressing intracellular reactive oxygen species and pro-inflammatory cytokines. In zebrafish, THRCI reduced oxidative stress and alleviated UV-induced caudal fin atrophy. In a murine model of acute UV photodamage, topical THRCI accelerated epidermal recovery, restored hydration and barrier function, increased dermal density, and promoted collagen fiber remodeling, while downregulating IL-6, IL-1β, MMP-1, and MMP-9. Collectively, these findings indicate that THRCI exhibits effective photodamage-repair properties in our established models and represents a promising animal-free collagen biomaterial for skin regeneration.

Graphical Abstract