articleRedox BiologyJan 6, 2026GOLD OA

RIPK3-driven phosphorylation of MFN2 orchestrates endoplasmic reticulum-mitochondria interaction and cardiomyocyte stress responses

Qingdao University · Affiliated Hospital of Qingdao University · +1 more institution

PubMed
Indexed incrossrefdoajpubmed

Abstract

Recent studies have demonstrated that necroptosis is one of the main forms of cardiomyocyte death in heart diseases. However, the crosstalk between the death-receptor necroptosis pathway and the mitochondrial necroptosis pathway remains largely unknown. It has been reported that Mitofusin 2 (MFN2) can promote myocardial injury by inducing Endoplasmic Reticulum (ER)-mitochondria interaction. The purpose of this study was to investigate whether MFN2 promotes cardiac necroptosis and myocardial ischemia/reperfusion (I/R) injury by regulating ER-mitochondrial interactions, and whether this function of MFN2 can be regulated by the death-receptor necroptosis pathway. Myocardial necroptosis was induced by H 2 O 2 in…

Citation impact

4
total citations
FWCI
41.74
Percentile
100%
References
49
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Authors

10

Topics & keywords

Keywords
  • Phosphorylation
  • MFN2
  • Endoplasmic reticulum
  • Mitochondrion
  • Kinase
  • Unfolded protein response
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