Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG20106)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
rno-miR-375-3p
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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Phospholipid hydroperoxide glutathione peroxidase (GPX4) [Suppressor]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Target for Ferroptosis | Suppressor | ||||
Responsed Disease | Ischemia/reperfusion injury | ICD-11: DB98 | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
rMTs (Rat myocardial tissues) | ||||
hCFs (Cardiac Fibroblasts) | |||||
In Vivo Model |
Forty-two SD rats were randomly divided into sham operation group (n = 6) and I/R model group (n = 36). In the model group, rats were ligated with left anterior descending coronary artery to simulate MI. Specifically, after anesthetizing the animals in the I/R model group, an oblique incision was made in the third and fourth intercostal spaces of the left chest to expose the heart. Under a stereomicroscope, the junction of the pulmonary artery cone and the left atrial appendage was ligated with 6/0 noninvasive suture needle silk threads at 1-2 mm below the starting point of the coronary artery. Successful ischemia was indicated by ST segment elevation or T wave height and peaks of MI performance on electrocardiogram (ECG). The ligation was stopped after 45 minutes of ischemia, and the rats were maintained for 24 hours after reperfusion. As a drug treatment, 6 I/R model rats were treated with 20 nmol miRNA NC inhibitor (Thermo Fisher Scientific, Waltham, MA), 20 nmol miR-375-3p antagomir (Thermo Fisher Scientific, Waltham, MA) and 2 mg/kg Ferrostatin-1 (Fer-1; MCE, USA) for 28 days. The myocardial tissues of rats in the sham operation and I/R model groups as well as I/R model drug treatment group were then used for subsequent testing.
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Response regulation | MiR-375-3p is an important factor inducing myocardial fibrosis after Myocardial infarction, which accelerates the ferroptosis of cardiomyocytes and promotes fibrosis by down-regulating GPX4. | ||||
Ischemia/reperfusion injury [ICD-11: DB98]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | rno-miR-375-3p (miRNA) | miRNA | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
rMTs (Rat myocardial tissues) | ||||
hCFs (Cardiac Fibroblasts) | |||||
In Vivo Model |
Forty-two SD rats were randomly divided into sham operation group (n = 6) and I/R model group (n = 36). In the model group, rats were ligated with left anterior descending coronary artery to simulate MI. Specifically, after anesthetizing the animals in the I/R model group, an oblique incision was made in the third and fourth intercostal spaces of the left chest to expose the heart. Under a stereomicroscope, the junction of the pulmonary artery cone and the left atrial appendage was ligated with 6/0 noninvasive suture needle silk threads at 1-2 mm below the starting point of the coronary artery. Successful ischemia was indicated by ST segment elevation or T wave height and peaks of MI performance on electrocardiogram (ECG). The ligation was stopped after 45 minutes of ischemia, and the rats were maintained for 24 hours after reperfusion. As a drug treatment, 6 I/R model rats were treated with 20 nmol miRNA NC inhibitor (Thermo Fisher Scientific, Waltham, MA), 20 nmol miR-375-3p antagomir (Thermo Fisher Scientific, Waltham, MA) and 2 mg/kg Ferrostatin-1 (Fer-1; MCE, USA) for 28 days. The myocardial tissues of rats in the sham operation and I/R model groups as well as I/R model drug treatment group were then used for subsequent testing.
Click to Show/Hide
|
||||
Response regulation | MiR-375-3p is an important factor inducing myocardial fibrosis after Myocardial infarction, which accelerates the ferroptosis of cardiomyocytes and promotes fibrosis by down-regulating GPX4. | ||||