Evidence map›Paper›PMID 41640247›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Targeted Mitochondrial ECSIT Overexpression Attenuates MASH by Increasing OTUD3 Expression.

Yuqing Jiang, Tingting Tong, Pengxi Shi, Xiaofan Chen, Chenhao Wang, Qingyuan Weng, Sihan Chen, Linli Que, Qi Chen, Yuehua Li and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

1 citing paper in PubMed.

  1. Review
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

12 authors.

Yuqing JiangKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, School of Basic Medical Science, Nanjing Medical University, Nanjing, Jiangsu, China.
Tingting TongKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, School of Basic Medical Science, Nanjing Medical University, Nanjing, Jiangsu, China.
Pengxi ShiKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, School of Basic Medical Science, Nanjing Medical University, Nanjing, Jiangsu, China.
Xiaofan ChenKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, School of Basic Medical Science, Nanjing Medical University, Nanjing, Jiangsu, China.
Chenhao WangKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, School of Basic Medical Science, Nanjing Medical University, Nanjing, Jiangsu, China.
Qingyuan WengThe First Clinical Medical College, Nanjing Medical University, Nanjing, Jiangsu, China.
Sihan ChenThe First Clinical Medical College, Nanjing Medical University, Nanjing, Jiangsu, China.
Linli QueKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, School of Basic Medical Science, Nanjing Medical University, Nanjing, Jiangsu, China.
Qi ChenKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, School of Basic Medical Science, Nanjing Medical University, Nanjing, Jiangsu, China.
Yuehua LiKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, School of Basic Medical Science, Nanjing Medical University, Nanjing, Jiangsu, China.
Qiang ZhuDepartment of Organ Transplantation, Eastern Hepatobiliary Surgery Hospital, Naval Medical University, Shanghai, China.
Jiantao LiKey Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, School of Basic Medical Science, Nanjing Medical University, Nanjing, Jiangsu, China.ORCID https://orcid.org/0009-0008-3487-7915

Funding

National Natural Science Foundation of China 81900221Natural Science Foundation of Shanghai City 25ZR1401391
6 · The paper itself

Abstract

Mitochondrial dysfunction plays a key role in the pathogenesis of metabolic dysfunction-associated steatohepatitis (MASH). As is known to play a key role in mitochondria, ECSIT, in relation to oxidized mitochondrial DNA is still unclear. This study examines mitochondrial ECSIT expression in MASH mouse models. Mitochondria-targeted ECSIT transgenic (ECSIT

Indexed as

Fatty LiverMitochondriaUbiquitin-Specific ProteasesAnimalsDisease Models, AnimalDNA, MitochondrialMiceMice, TransgenicSirtuin 3DNA, MitochondrialSirtuin 3Ubiquitin-Specific ProteasesECSITMASHOTUD3ox‐mtDNASIRT3

Identifiers

PMID41640247
PMCPMC13088300

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.