Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG20105)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
rno-miR-335
can regulate the following target(s), and cause disease/drug response(s). You can browse detail information of target(s) or disease/drug response(s).
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Ferritin heavy chain (FTH1) [Suppressor; Marker]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Target for Ferroptosis | Marker/Suppressor | ||||
Responsed Disease | Parkinson disease | ICD-11: 8A00 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
PC12 cells | Adrenal gland pheochromocytoma | Rattus norvegicus | CVCL_0481 | |
In Vivo Model |
A total of 48 male Sprague-Dawley rats (weighing, 180-220 g; 6-8 weeks of age) were purchased from the Animal Center of Guangzhou University of Chinese Medicine (Guangzhou, China). The rats were anesthetized (100 mg/kg ketamine and 10 mg/kg xylazine, intraperitoneal injection) and placed in a stereotaxic apparatus with the skull flat. An intracerebral injection of 6-OHDA was performed at 2 sites in the right SN pars compacta (SNpc) and ventral tegmental area (VTA): Anteroposterior (A/P)=-4.9 mm; mediolateral (M/L)=-1.9 mm; dorsoventral (D/V)=-7.5 mm; and anteroposterior (A/P)=-4.9 mm; mediolateral (M/L)=-1.1 mm; dorsoventral (D/V)=8.0 mm. During the surgery, body temperature was maintained at ~36.5 using a heating pad. All rats received meticulous post-operative care.
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Response regulation | MiR335 promotes ferroptosis by targeting FTH1 inin vitroandin vivomodels of Parkinson's disease, providing a potential therapeutic target for the treatment of PD. Mechanistically, miR335 enhanced ferroptosis through the degradation of FTH1 to increase iron release, lipid peroxidation and reactive oxygen species (ROS) accumulation, and to decrease mitochondrial membrane potential (MMP). | ||||
Parkinson disease [ICD-11: 8A00]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | rno-miR-335 (miRNA) | miRNA | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
PC12 cells | Adrenal gland pheochromocytoma | Rattus norvegicus | CVCL_0481 | |
In Vivo Model |
A total of 48 male Sprague-Dawley rats (weighing, 180-220 g; 6-8 weeks of age) were purchased from the Animal Center of Guangzhou University of Chinese Medicine (Guangzhou, China). The rats were anesthetized (100 mg/kg ketamine and 10 mg/kg xylazine, intraperitoneal injection) and placed in a stereotaxic apparatus with the skull flat. An intracerebral injection of 6-OHDA was performed at 2 sites in the right SN pars compacta (SNpc) and ventral tegmental area (VTA): Anteroposterior (A/P)=-4.9 mm; mediolateral (M/L)=-1.9 mm; dorsoventral (D/V)=-7.5 mm; and anteroposterior (A/P)=-4.9 mm; mediolateral (M/L)=-1.1 mm; dorsoventral (D/V)=8.0 mm. During the surgery, body temperature was maintained at ~36.5 using a heating pad. All rats received meticulous post-operative care.
Click to Show/Hide
|
||||
Response regulation | MiR335 promotes ferroptosis by targeting FTH1 inin vitroandin vivomodels of Parkinson's disease, providing a potential therapeutic target for the treatment of PD. Mechanistically, miR335 enhanced ferroptosis through the degradation of FTH1 to increase iron release, lipid peroxidation and reactive oxygen species (ROS) accumulation, and to decrease mitochondrial membrane potential (MMP). | ||||