Evidence map›Paper›PMID 42048853›Full record

ArticleJACC. Basic to translational science2026

Systems Biology Identifies TARS2 as a Cardiomyocyte Regulator of Mitochondrial Oxidative Stress in Dilated Cardiomyopathy.

Liming Chen, Xuan Li, Xiaolei Sun, Xiaolin Wang, Jian Wu, Enyong Su, Shijun Wang, Huan Sun, Leilei Ma, Yunzeng Zou

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JACC. Basic to translational science, 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. Article
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

10 authors.

Liming ChenDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China; State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China; Centre for Cardiovascular Science, Queen's Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Xuan LiDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China; State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
Xiaolei SunDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China; State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
Xiaolin WangDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China; State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
Jian WuDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China; State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
Enyong SuDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China; State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
Shijun WangDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China; State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
Huan SunCardiology Department, China-Japan Union Hospital of Jilin University, Changchun, China.
Leilei MaDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China; State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China. Electronic address: mllsdjn@yahoo.com.
Yunzeng ZouDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institute of Biomedical Sciences, Fudan University, Shanghai, China; State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China. Electronic address: zou.yunzeng@zs-hospital.sh.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dilated cardiomyopathy (DCM), a leading cause of heart failure, is characterized by progressive cardiomyocyte (CM) loss and mitochondrial dysfunction; yet, the molecular drivers of mitochondrial oxidative stress (MitOS) remain unclear. By integrating bulk, single-cell, and spatial transcriptomics with machine learning, we identified threonyl-tRNA synthetase 2 (TARS2) as a CM-enriched regulator of MitOS. TARS2 was consistently up-regulated in human DCM hearts and associated with apoptotic signaling and enhanced macrophage crosstalk. Functional studies demonstrated that TARS2 overexpression disrupted mitochondrial homeostasis, triggered excessive mitochondrial reactive oxygen species, and induced CM apoptosis, whereas genetic inhibition restored mitochondrial function, reduced apoptosis, and improved cardiac performance. These findings uncover TARS2 as a novel regulator of mitochondrial dysfunction and pathological remodeling in DCM, providing both mechanistic insights and therapeutic implications, and establish a systems biology framework for translational discovery of disease targets in cardiovascular medicine.

Indexed as

dilated cardiomyopathyheart failuremitochondrial oxidative stressTARS2transcriptomic analyses

Identifiers

PMID42048853
PMCPMC13138171

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.