ArticleNature communications2025
5-ALA photodynamic metabolite-powered zero-waste ferroptosis amplifier for enhanced hypertrophic scar therapy.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Blastocyst-Derived Lactic Acid Regulates Uterine Epithelial Receptivity and Stromal Decidualization via the HIF1α-HO-1-Heme Metabolic Axis.Antioxidants (Basel, Switzerland) · 2026Article
- A Photothermally Amplified Enzyme-Nitric Oxide Co-Regulatory System Reprograms Pathological ECM-Fibroblast Crosstalk to Alleviate Hypertrophic Scarring.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Epigenetic orchestration of scar formation: Therapeutic potential of targeting DNA methylation and non‑coding RNAs in cutaneous fibrosis (Review).Molecular medicine reports · 2026Review
- Rational design of FAP-targeted sEVs delivered by microneedles for precision treatment of hypertrophic scars via ferroptosis in hypertrophic scar fibroblasts.Materials today. Bio · 2026Article
- Metal-dependent regulated cell death: Molecular architecture and translational frontiers.iMeta · 2026Review
- Research advances in the pathogenesis and photodynamic therapy of pathological scars.Lasers in medical science · 2026Review
- Ferroptosis-autophagy crosstalk in bladder cancer: mechanisms and therapeutic implications.Molecular cancer · 2026Review
- Advanced applications of cationic photosensitizer DHPC in photodynamic eradication of drug-resistant bacteria.Frontiers in microbiology · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Hypertrophic scars are a stubborn form of dermal fibrosis that impairs quality of life. Although 5-ALA-mediated photodynamic therapy holds promise, its efficacy is undermined by poor transdermal delivery and rapid metabolism into non-photosensitive heme. Here, we introduce a "zero-waste" strategy that repurposes 5-ALA-derived heme to synergistically amplify ferroptosis. This is achieved by co-encapsulating 5-ALA and baicalin within human H-ferritin, subsequently incorporated into polyvinylpyrrolidone microneedles. The resulting system enables targeted delivery to hypertrophic scar fibroblasts with pH-responsive, programmable drug release. Upon administration, 5-ALA generates protoporphyrin IX to initiate photodynamic therapy. Baicalin is then released to induce ferroptosis and synergize with the reactive oxygen species and heme accumulated during photodynamic therapy, thereby overstimulating the HO-1-heme metabolic axis. This cascade promotes the release of Fe²⁺ and CO, further amplifying ferroptotic responses. Moreover, the ferroptotic stress triggers mitophagy and mitochondrial Fe²⁺ efflux. By harnessing 5-ALA metabolic byproducts, this strategy achieved markedly prolonged anti-scar efficacy in the female rabbit ear HS tissues, surpassing that of conventional therapies.
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