Ferroptosis-centered Disease Response Information
General Information of the Disease (ID: DIS00090)
Name |
Extraocular muscles disorder
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ICD |
ICD-11: 9C82
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Full List of Target(s) of This Ferroptosis-centered Disease
Nuclear factor erythroid 2-related factor 2 (NFE2L2)
In total 1 item(s) under this target | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [1] | |||
Target for Ferroptosis | Marker/Suppressor | |||
Responsed Disease | Ocular fibrosis [ICD-11: 9C82.2] | |||
Responsed Drug | Artesunate | Investigative | ||
Pathway Response | Ferroptosis | hsa04216 | ||
PI3K-Akt signaling pathway | hsa04151 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | hOFs (Human ocular fibroblasts) | |||
Response regulation | Expression of mitochondrial GPX4 but no other forms of GPX4 was decreased after artesunate treatment and that mitochondrial GPX4 overexpression rescued artesunate-induced lipid peroxidation and ferroptosis. Other cellular ferroptosis defense mechanisms, including cellular FSP1 and Nrf2, were also inhibited by artesunate. In conclusion, our study demonstrated that artesunate protects against fibrosis through abrogation of fibroblast activation and induction of mitochondria-dependent ferroptosis in ocular fibrosis, which may offer a potential treatment for ocular fibrosis. | |||
Ferroptosis suppressor protein 1 (AIFM2)
In total 1 item(s) under this target | ||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target | [1] | |||
Target for Ferroptosis | Suppressor | |||
Responsed Disease | Ocular fibrosis [ICD-11: 9C82.2] | |||
Responsed Drug | Artesunate | Investigative | ||
Pathway Response | Ferroptosis | hsa04216 | ||
PI3K-Akt signaling pathway | hsa04151 | |||
Cell Process | Cell ferroptosis | |||
In Vitro Model | hOFs (Human ocular fibroblasts) | |||
Response regulation | Expression of mitochondrial GPX4 but no other forms of GPX4 was decreased after artesunate treatment and that mitochondrial GPX4 overexpression rescued artesunate-induced lipid peroxidation and ferroptosis. Other cellular ferroptosis defense mechanisms, including cellular FSP1 and Nrf2, were also inhibited by artesunate. In conclusion, our study demonstrated that artesunate protects against fibrosis through abrogation of fibroblast activation and induction of mitochondria-dependent ferroptosis in ocular fibrosis, which may offer a potential treatment for ocular fibrosis. | |||