Retinol saturase in the mitochondria antagonizes IDH2 and GLUD1 acetylation to mediate heart repair

inhibits heart regeneration in neonatal mice. Surprisingly, Retsat drives cardiomyocyte proliferation independently of its classical retinol saturase activity in the ER. Retsat also localizes in cardiomyocyte mitochondria, and mitochondrial-specific overexpression of Retsat can stimulate cardiomyocyte proliferation and heart repair after injury. Mechanistically, Retsat in the mitochondria acts as an antagonist of Idh2 and Glud1 acetylation, reducing their acetylation levels and enhancing their activities. Furthermore, Retsat enters mitochondria by interacting with Tom70 and Tim23 proteins. These data suggest that targeting Retsat is a promising strategy for promoting cardiac regeneration after heart injury.

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Publication Details

Journal
Proceedings of the National Academy of Sciences
Published
2026-03-31
DOI
https://doi.org/10.1073/pnas.2526203123
Primary Topic
Endoplasmic Reticulum Stress and Disease
Type
article
Field-Weighted Citation Impact
0.00

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article

Retinol saturase in the mitochondria antagonizes IDH2 and GLUD1 acetylation to mediate heart repair

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Proceedings of the National Academy of Sciences
Endoplasmic Reticulum Stress and Disease
article

Retinol saturase in the mitochondria antagonizes IDH2 and GLUD1 acetylation to mediate heart repair

Hongyang Chen, Yuqing Lin, Xinlu Gao, Yanan Tian, HANJING LI, Zhongyu Ren, Yining Liu, Xin Wang, Qimeng Ouyang, Zhenwei Pan, Yu Hu, Wenya Ma, Lei Xu, Yu Liu, Ye Tian, Jianglong Li
article en

Abstract

inhibits heart regeneration in neonatal mice. Surprisingly, Retsat drives cardiomyocyte proliferation independently of its classical retinol saturase activity in the ER. Retsat also localizes in cardiomyocyte mitochondria, and mitochondrial-specific overexpression of Retsat can stimulate cardiomyocyte proliferation and heart repair after injury. Mechanistically, Retsat in the mitochondria acts as an antagonist of Idh2 and Glud1 acetylation, reducing their acetylation levels and enhancing their activities. Furthermore, Retsat enters mitochondria by interacting with Tom70 and Tim23 proteins. These data suggest that targeting Retsat is a promising strategy for promoting cardiac regeneration after heart injury.

Proceedings of the National Academy of SciencesVol. 123(14)
Ministry of Education of the People's Republic of China (CN), Harbin Medical University (CN), National Health and Family Planning Commission (CN), Fourth Affiliated Hospital of Harbin Medical University (CN), Research Institute of General Pathology and Pathophysiology, the Russian Academy of Medical Sciences (RU), Second Affiliated Hospital of Harbin Medical University (CN)
National Natural Science Foundation of China, Natural Science Foundation of Heilongjiang Province
Good health and well-being
Openalex Percentile: Top 39%
Endoplasmic Reticulum Stress and Disease
DOIOpen Access PDFOpenAlex
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