Ferroptosis-centered Drug Response Information
General Information of the Drug (ID: ferrodrug0381)
Name |
Carbonyl cyanide-m-chlorophenyl-hydrazine
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Drug Type |
Small molecule
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Full List of Ferroptosis Target Related to This Drug
Phospholipid hydroperoxide glutathione peroxidase (GPX4)
In total 1 item(s) under this Target | |||||
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target | [1] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Osteoporosis | ICD-11: FB83 | |||
Responsed Regulator | Ferritin, mitochondrial (FTMT) | Suppressor | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Autophagy | hsa04140 | ||||
Cell Process | Cell ferroptosis | ||||
Cell autophagy | |||||
In Vitro Model | hFOB 1.19 cells | Normal | Homo sapiens | CVCL_3708 | |
In Vivo Model |
Forty-five SD rats (3 months old, 200 ± 20 g) were obtained from the Department of Experimental Animals in China Medical University (Animal Certificate Number: SCXK (Liaoning) 2008-0005). Fifteen rats grew as control while other thirty rats were established T2DOP model. The model rats were given a high-fat feed and 12 h/day water for 2 months. Then streptozotocin was intraperitoneally injected at 30 mg/kg. Seventy-two hours later, the model was successfully established when insulin sensitivity index decreased and fasting plasma glucose exceeded 7.8 mmol/L. Then all rats continue grew 3 months to cause osteoporosis. Thirty model rats were divided into two groups. One was fifteen T2DOP rats only, and other was fifteen T2DOP rats with deferoxamine (DFO) treatment (60 mg/kg/day, intraperitoneally inject, last for the last 1 month).
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Response regulation | Carbonyl cyanide-m-chlorophenyl-hydrazine (CCCP) is a mitophagy agonist. Through adding mitophagy agonist CCCP to osteoblasts, we found the increase of ROS and lipid peroxidation while GPX4 decreased. FtMt inhibited the occurrence of ferroptosis in osteoblasts by reducing oxidative stress caused by excess ferrous ions, and FtMt deficiency induced mitophagy in the pathogenesis of type 2 diabetic osteoporosis (T2DOP). | ||||