Journal of photochemistry and photobiology. B, Biology · 2025
Hypericin-mediated photodynamic therapy promotes apoptosis and inhibits fibrosis by inducing HMOX1-mediated ferroptosis in hypertrophic scar fibroblasts.
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Li Xing, Chen Ziqing, Liu Mingzhuo, An Jingwen, Shang Jinwei, Zhu Gehua, Wen Huicai, Guo Guanghua
Аннотация
BACKGROUND: The treatment of hypertrophic scars poses a significant therapeutic challenge due to the limitations of existing options. Given the inadequacy of current regimens, it is imperative to explore new and more effective treatment strategies.
OBJECTIVE: Here, we investigated the mechanism by which hypericin-mediated photodynamic therapy (HYP-PDT) inhibits hypertrophic scar formation, with a focus on the role of HMOX1 and ferroptosis.
METHODS: Using hypertrophic scar fibroblasts (HFs), we determined optimal HYP-PDT conditions and assessed its effects on cell proliferation, migration, apoptosis, and fibrosis. Integrated transcriptomic and proteomic analyses were performed to identify key targets, followed by mechanistic studies on ferroptosis.
RESULTS: HYP-PDT significantly suppressed HF proliferation, migration, and fibrotic protein expression, while promoting apoptosis. Multi-omics analysis identified HMOX1 as a key upregulated target linked to ferroptosis. HYP-PDT increased ROS, lipid peroxidation, and Fe2+ levels-effects reversible by ferroptosis inhibitors. HMOX1 overexpression enhanced HYP-PDT-induced ferroptosis and apoptosis, but alone did not trigger these processes.
CONCLUSION: This study demonstrates that HYP-PDT induces ferroptosis via HMOX1 upregulation, providing a new mechanistic basis and potential therapeutic target for hypertrophic scar management.
OBJECTIVE: Here, we investigated the mechanism by which hypericin-mediated photodynamic therapy (HYP-PDT) inhibits hypertrophic scar formation, with a focus on the role of HMOX1 and ferroptosis.
METHODS: Using hypertrophic scar fibroblasts (HFs), we determined optimal HYP-PDT conditions and assessed its effects on cell proliferation, migration, apoptosis, and fibrosis. Integrated transcriptomic and proteomic analyses were performed to identify key targets, followed by mechanistic studies on ferroptosis.
RESULTS: HYP-PDT significantly suppressed HF proliferation, migration, and fibrotic protein expression, while promoting apoptosis. Multi-omics analysis identified HMOX1 as a key upregulated target linked to ferroptosis. HYP-PDT increased ROS, lipid peroxidation, and Fe2+ levels-effects reversible by ferroptosis inhibitors. HMOX1 overexpression enhanced HYP-PDT-induced ferroptosis and apoptosis, but alone did not trigger these processes.
CONCLUSION: This study demonstrates that HYP-PDT induces ferroptosis via HMOX1 upregulation, providing a new mechanistic basis and potential therapeutic target for hypertrophic scar management.