Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG20083)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
mmu-miR-351-3p
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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Unspecific Target [Unspecific Target]
| In total 1 item(s) under this target | |||||
| Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
| Responsed Disease | Chronic heart failure | ICD-11: BD1Z | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Necroptosis | hsa04217 | ||||
| NF-kappa B signaling pathway | hsa04064 | ||||
| Cell Process | Cell ferroptosis | ||||
| Cell pyroptosis | |||||
In Vitro Model |
rHTs (Rat hippocampal tissues) | ||||
| In Vivo Model |
Male wild-type (WT) C57BL/6J mice aged 8 weeks were obtained from the Experimental Animal Center, Guangzhou University of Chinese Medicine. Sham and TAC mice received corresponding isotype i.p. injections. TAC + AAVMLK3- mice were generated by intravenous (i.v.) injection of adeno-associated viral vector-MLK3 vector (AAVMLK3-) (GenePharma, Shanghai, China) 14 and 21 days before TAC surgery. Sham + AAVNC and TAC + AAVNC mice received AAVNC i.v. injections. TAC + antagomir and TAC + agomir were generated by i.v. injection of antagomir and agomir (30 pmol/g) 14 and 21 days before TAC surgery, respectively.
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| Response regulation | MLK3 (MAP3K11) mainly regulates the JNK/p53 signaling pathway-mediated oxidative stress and that ferroptosis causes myocardial fibrosis in the advanced stages of chronic heart failure (CHF). Promoting the expression of miR-351 can inhibit the expression of MLK3, and significantly improve cardiac function in mice subjected to TAC. | ||||
Chronic heart failure [ICD-11: BD1Z]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | mmu-miR-351-3p (miRNA) | miRNA | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Ferroptosis | hsa04216 | ||||
| Necroptosis | hsa04217 | ||||
| NF-kappa B signaling pathway | hsa04064 | ||||
| Cell Process | Cell ferroptosis | ||||
| Cell pyroptosis | |||||
In Vitro Model |
rHTs (Rat hippocampal tissues) | ||||
| In Vivo Model |
Male wild-type (WT) C57BL/6J mice aged 8 weeks were obtained from the Experimental Animal Center, Guangzhou University of Chinese Medicine. Sham and TAC mice received corresponding isotype i.p. injections. TAC + AAVMLK3- mice were generated by intravenous (i.v.) injection of adeno-associated viral vector-MLK3 vector (AAVMLK3-) (GenePharma, Shanghai, China) 14 and 21 days before TAC surgery. Sham + AAVNC and TAC + AAVNC mice received AAVNC i.v. injections. TAC + antagomir and TAC + agomir were generated by i.v. injection of antagomir and agomir (30 pmol/g) 14 and 21 days before TAC surgery, respectively.
Click to Show/Hide
|
||||
| Response regulation | MLK3 (MAP3K11) mainly regulates the JNK/p53 signaling pathway-mediated oxidative stress and that ferroptosis causes myocardial fibrosis in the advanced stages of chronic heart failure (CHF). Promoting the expression of miR-351 can inhibit the expression of MLK3, and significantly improve cardiac function in mice subjected to TAC. | ||||