Disrupted Mitochondrial Dynamics Impair Corneal Epithelial Healing in Neurotrophic Keratopathy DOI Open Access

Mengyi Jin,

Zeyu Liu, Ruize Shi

и другие.

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(3), С. 1290 - 1290

Опубликована: Фев. 3, 2025

Neurotrophic keratopathy (NK) is a degenerative corneal disease characterized by impaired sensitivity and epithelial repair that often linked to sensory nerve dysfunction. To establish clinically relevant model explore the mechanisms underlying NK pathogenesis, we developed novel mouse through partial transection of ciliary nerve. This approach mimics progressive nature NK, reproducing key clinical features such as defects, reduced sensitivity, diminished tear secretion, delayed wound healing. Using this model, investigated how disruptions in mitochondrial dynamics contribute dysfunction NK. Our findings revealed substantial dynamics, including expression fusion proteins (OPA1), downregulation fission regulators (FIS1 MFF), transport, evidenced decreased Rhot1 Kif5b. Additionally, mitophagy-related genes (Pink1 Prkn) contributed accumulation dysfunctional mitochondria, leading DNA damage repair. These abnormalities were accompanied increased γH2AX staining, indicative double-strand breaks cellular stress. study highlights pivotal role health repair, suggesting therapeutic strategies aimed at restoring function, enhancing mitophagy, mitigating oxidative stress may offer promising avenues for treating

Язык: Английский

Disrupted Mitochondrial Dynamics Impair Corneal Epithelial Healing in Neurotrophic Keratopathy DOI Open Access

Mengyi Jin,

Zeyu Liu, Ruize Shi

и другие.

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(3), С. 1290 - 1290

Опубликована: Фев. 3, 2025

Neurotrophic keratopathy (NK) is a degenerative corneal disease characterized by impaired sensitivity and epithelial repair that often linked to sensory nerve dysfunction. To establish clinically relevant model explore the mechanisms underlying NK pathogenesis, we developed novel mouse through partial transection of ciliary nerve. This approach mimics progressive nature NK, reproducing key clinical features such as defects, reduced sensitivity, diminished tear secretion, delayed wound healing. Using this model, investigated how disruptions in mitochondrial dynamics contribute dysfunction NK. Our findings revealed substantial dynamics, including expression fusion proteins (OPA1), downregulation fission regulators (FIS1 MFF), transport, evidenced decreased Rhot1 Kif5b. Additionally, mitophagy-related genes (Pink1 Prkn) contributed accumulation dysfunctional mitochondria, leading DNA damage repair. These abnormalities were accompanied increased γH2AX staining, indicative double-strand breaks cellular stress. study highlights pivotal role health repair, suggesting therapeutic strategies aimed at restoring function, enhancing mitophagy, mitigating oxidative stress may offer promising avenues for treating

Язык: Английский

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