[ROMO1 Promotes the Repair of Radiation-induced Skin Injury by Regulating Mitochondrial Function and Keratinocyte Proliferation].
Rattachement africain : cn, République démocratique du Congo. Niveau de preuve : code pays fourni par la source.
Le résumé fourni par la source
Objective: To investigate the molecular mechanisms of early mitochondrial stress in keratinocytes induced by ionizing radiation (IR), focusing on the key role of ROMO1 in radiation-induced skin injury (RISI). Methods: -sKO mice. Results: -sKO mice showed accelerated wound healing, with a reduction in skin injury score by approximately 1 point, along with enhanced tissue regeneration at 25 days post-irradiation compared to control mice. Conclusion: The mitochondrial protein ROMO1 is a key regulator of the early keratinocyte stress response to radiation. It impedes the repair of radiation-induced skin injury by suppressing cell proliferation via modulation of mitochondrial function. Targeted inhibition of ROMO1 may represent a novel therapeutic strategy to promote healing and prevent chronic progression of radiation-induced skin injury.
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