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

Our findings reveal that RIPK3 can mediate MFN2 phosphorylation to promote ER-mitochondria interaction and mitochondrial Ca<sup>2+</sup> overload, leading to the induction of cardiac necroptosis.

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Publication Details

Journal
Redox Biology
Published
2026-01-06
DOI
https://doi.org/10.1016/j.redox.2026.104006
Primary Topic
Mitochondrial Function and Pathology
Type
article
Field-Weighted Citation Impact
0.00
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article

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

Peiyan Wang, Tao Xu, Xiang Ao, P. Wang et al.
Redox Biology
Mitochondrial Function and Pathology
article

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

Peiyan Wang, Tao Xu, Xiang Ao, P. Wang, Qing Li, Lin Ye, Wei Ding, Yanru Wang, Yihan Song, Jianxun Wang
article en

Abstract

Our findings reveal that RIPK3 can mediate MFN2 phosphorylation to promote ER-mitochondria interaction and mitochondrial Ca<sup>2+</sup> overload, leading to the induction of cardiac necroptosis.

Redox BiologyVol. 90
Qingdao University (CN), Qingdao Agricultural University (CN), Affiliated Hospital of Qingdao University (CN)
Openalex Percentile: Top 96%
Mitochondrial Function and Pathology
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RIPK3-driven phosphorylation of MFN2 orchestrates endoplasmic reticulum-mitochondria interaction and cardiomyocyte stress responses — Peiyan Wang, Tao Xu, et al. · Redox Biology (2026) | TGRS Research Map | TGRS