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

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 The alternative text for this image may have been generated using AI.