METTL3 boosts mitochondrial fission and induces cardiac fibrosis after ischemia/reperfusion injury
Li Ma, Xing Chang, Jing Gao, Ying Zhang, Ye Chen, H. Zhou, Na Zhou, Na Du, Jiamin Li, Jiachen Bi, Ziyue Chen, Xinxin Chen, Qingyong He
Abstract
deficiency interfere with DNA-PKcs phosphorylation, thereby blocking the downstream activation of Fis1 and preventing pathological mitochondrial fission. In conclusion, this study confirms that inhibition of METTL3 can alleviate myocardial cardiac fibrosis inflammation and prevent cardiomyocyte death under reperfusion injury conditions by disrupting DNA-PKcs/Fis1-dependent mitochondrial fission, ultimately improving cardiac function. These findings suggest new approaches for clinical intervention in patients with MIRI.
Topics & Concepts
Mitochondrial fissionFIS1Reperfusion injuryFibrosisCardiac fibrosisMedicineInflammationMitochondrionIschemiaPharmacologyCardiologyInternal medicineCell biologyBiologyMitochondrial DNAmitochondrial fusionBiochemistryGeneRNA modifications and cancerMitochondrial Function and PathologyFuel Cells and Related Materials