Evidence map›Paper›PMID 41915751›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2026

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

Wenya Ma, Yanan Tian, Jianglong Li, Qimeng Ouyang, Lei Xu, Bowei Zhang, Hongyang Chen, Hanjing Li, Yuqing Lin, Yu Hu and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors.

Wenya Ma *Department of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Yanan Tian *Department of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Jianglong Li *Department of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Qimeng Ouyang *Department of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Lei XuDepartment of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Bowei ZhangDepartment of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Hongyang ChenDepartment of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Hanjing LiDepartment of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Yuqing LinDepartment of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Yu HuDepartment of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Zhongyu RenDepartment of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Yifu ShenDepartment of Laboratory Medicine at The Fourth Affiliated Hospital, Harbin Medical University, Harbin 150086, China.ORCID 0009-0009-2597-8383
Xin WangDepartment of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Xinlu GaoDepartment of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Xiuxiu WangDepartment of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Yining LiuDepartment of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.
Ye TianDepartment of Pathophysiology and the Key Laboratory of Cardiovascular Pathophysiology, Harbin Medical University, Harbin 150081, China.
Yu LiuDepartment of Laboratory Medicine at The Fourth Affiliated Hospital, Harbin Medical University, Harbin 150086, China.ORCID 0000-0003-1772-098X
Zhenwei PanDepartment of Pharmacology at College of Pharmacy (The Key Laboratory of Cardiovascular Research, Ministry of Education, National Key Laboratory of Frigid Zone Cardiovascular Diseases), Harbin Medical University, Harbin 150086, China.
Benzhi CaiDepartment of Pharmacy at the Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.ORCID 0000-0003-0017-867X

Funding

Heilongjiang Provincial Natural Science Foundation of China PL2024H083Heilongjiang Provincial Natural Science Foundation of China ZL2024H017the National Natural Science Foundation of China 82100300 82470266The National Natural Science Foundation of China 92168119 82373958
6 · The paper itself

Abstract

Facilitating endogenous cardiomyocyte proliferation has emerged as an important strategy for cardiac repair. Conserved retinol saturase (Retsat) functions in producing all-trans 13,14-dihydroretinol in the endoplasmic reticulum (ER). However, Retsat's role and mechanism in heart regeneration remain unclear. Here, we uncover that Retsat is upregulated in cardiomyocytes during cardiac regeneration in mice. Cardiomyocyte-specific

Indexed as

HeartIsocitrate DehydrogenaseMitochondriaMitochondria, HeartAcetylationAnimalsCell ProliferationMiceMice, KnockoutMitochondrial ProteinsMyocytes, CardiacNerve Tissue ProteinsRegenerationBLOC1S1 protein, mouseIsocitrate Dehydrogenaseisocitrate dehydrogenase 2, mouseMitochondrial ProteinsNerve Tissue Proteinscardiomyocyte proliferationGlud1Idh2Retsat

Identifiers

PMID41915751
PMCPMC13056075

What Socratic holds

Textmetadata
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.