Evidence map›Paper›PMID 40711504›Full record

ArticleJournal of cardiovascular translational research2025

Single-Cell Sequencing Identifies the Crucial Role of Mitochondrial Fission-Fusion Imbalance in Heart Failure Progression.

Tao He, Jianmei Sha, Yuxin Hu, Caihong Shao, Yi Zhou, Lu Chen, Jianhua Yao, Junli Gao

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Journal of cardiovascular translational research, 2025. 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

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

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

8 authors.

Tao He *Cardiac Regeneration and Aging Lab, Institute of Geriatrics (Shanghai University), School of Life Science, Affiliated Nantong Hospital of Shanghai UniversityThe Sixth People's Hospital of Nantong) andShanghai University, Nantong, 226011, China.
Jianmei Sha *Shanghai University Hospital, Shanghai University, Shanghai, 200444, China.
Yuxin Hu *Cardiac Regeneration and Aging Lab, Institute of Geriatrics (Shanghai University), School of Life Science, Affiliated Nantong Hospital of Shanghai UniversityThe Sixth People's Hospital of Nantong) andShanghai University, Nantong, 226011, China.
Caihong ShaoDepartment of Internal Emergency Medicine, School of Medicine, Shanghai East Hospital, Tongji University, Shanghai, 200120, China.
Yi ZhouCardiac Regeneration and Aging Lab, Institute of Geriatrics (Shanghai University), School of Life Science, Affiliated Nantong Hospital of Shanghai UniversityThe Sixth People's Hospital of Nantong) andShanghai University, Nantong, 226011, China.
Lu ChenCardiac Regeneration and Aging Lab, Institute of Geriatrics (Shanghai University), School of Life Science, Affiliated Nantong Hospital of Shanghai UniversityThe Sixth People's Hospital of Nantong) andShanghai University, Nantong, 226011, China.
Jianhua YaoDepartment of Cardiology, School of Medicine, Tenth People's Hospital, Tongji University, Shanghai, 200090, China. jianhuayao@tongji.edu.cn.
Junli GaoCardiac Regeneration and Aging Lab, Institute of Geriatrics (Shanghai University), School of Life Science, Affiliated Nantong Hospital of Shanghai UniversityThe Sixth People's Hospital of Nantong) andShanghai University, Nantong, 226011, China. jlgao1@outlook.com.ORCID 0000-0002-8207-5545

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The heart grows in response to both pathological and physiological stimuli. Pathological hypertrophy often leads to cardiomyocyte loss and heart failure (HF), whereas physiological hypertrophy paradoxically protects the heart. Comparing these two types of hypertrophy can elucidate the differences and connections in their molecular mechanisms, which is pivotal for unraveling the pathogenesis of HF. This study compares pathological (TAC-induced) and physiological (exercise-induced) cardiac hypertrophy using single-cell and bulk transcriptomics. Mitochondrial fusion/fission imbalance emerged as a key dysregulated pathway in both models. An early increase in the fusion/fission ratio (2 weeks post-TAC) resembled exercise-induced remodeling, while a progressive decline at 5-8 weeks marked transition to pathological hypertrophy. By 11 weeks, suppressed fusion and increased fission led to heart failure. Downregulation of fusion genes (Mfn1, Mfn2, Opa1) and upregulation of fission genes (Fis1, Dnm1l) highlight mitochondrial dynamics as critical drivers of disease progression.

Indexed as

CardiomegalyHeart FailureMitochondria, HeartMitochondrial DynamicsMyocytes, CardiacSingle-Cell AnalysisTranscriptomeVentricular RemodelingAnimalsDisease Models, AnimalDisease ProgressionMaleMice, Inbred C57BLMitochondrial ProteinsRNA-SeqTime FactorsMitochondrial ProteinsHeart failureMitochondrial fissionMitochondrial fusionPathological hypertrophyPhysiological hypertrophySingle-cell transcriptomics

Identifiers

PMID40711504

What Socratic holds

Textmetadata
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.