Evidence map›Paper›PMID 25022898›Full record

ArticleCell research2014

Tom70 serves as a molecular switch to determine pathological cardiac hypertrophy.

Jun Li, Man Qi, Changming Li, Dan Shi, Dasheng Zhang, Duanyang Xie, Tianyou Yuan, Jing Feng, Yi Liu, Dandan Liang and 9 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
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

29 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Transmembrane protein 117 knockdown protects against angiotensin-II-induced cardiac hypertrophy.Hypertension research : official journal of the Japanese Society of Hypertension · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Tom70 protects against diabetic cardiomyopathy through its antioxidant and antiapoptotic properties.Hypertension research : official journal of the Japanese Society of Hypertension · 2020
    Article
  20. 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

19 authors at 1 institution in 1 country.

Jun Li1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Institute of Medical Genetics, Tongji University, Shanghai 200092, China.
Man Qi1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Department of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai 200120, China.
Changming Li1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Department of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai 200120, China.
Dan Shi1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Institute of Medical Genetics, Tongji University, Shanghai 200092, China.
Dasheng Zhang1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Institute of Medical Genetics, Tongji University, Shanghai 200092, China.
Duanyang Xie1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Department of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai 200120, China.
Tianyou Yuan1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Institute of Medical Genetics, Tongji University, Shanghai 200092, China.
Jing Feng1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Department of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai 200120, China.
Yi Liu1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Institute of Medical Genetics, Tongji University, Shanghai 200092, China.
Dandan Liang1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Institute of Medical Genetics, Tongji University, Shanghai 200092, China.
Xinran Xu1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Institute of Medical Genetics, Tongji University, Shanghai 200092, China.
Jinjin Chen1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Department of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai 200120, China.
Liang Xu1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Institute of Medical Genetics, Tongji University, Shanghai 200092, China.
Hong Zhang1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Institute of Medical Genetics, Tongji University, Shanghai 200092, China.
Jiangchuan Ye1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Department of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai 200120, China.
Fei Lv1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Department of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai 200120, China.
Jian Huang1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Department of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai 200120, China.
Luying PengDepartment of Pathology and Pathophysiology, Tongji University School of Medicine, Shanghai 200092, China.
Yi-Han Chen1] Key Laboratory of Basic Research in Cardiology of the Ministry of Education of China, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [2] Institute of Medical Genetics, Tongji University, Shanghai 200092, China [3] Department of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai 200120, China [4] Department of Pathology and Pathophysiology, Tongji University School of Medicine, Shanghai 200092, China.
Tongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathological cardiac hypertrophy is an inevitable forerunner of heart failure. Regardless of the etiology of cardiac hypertrophy, cardiomyocyte mitochondrial alterations are always observed in this context. The translocases of mitochondrial outer membrane (Tom) complex governs the import of mitochondrial precursor proteins to maintain mitochondrial function under pathophysiological conditions; however, its role in the development of pathological cardiac hypertrophy remains unclear. Here, we showed that Tom70 was downregulated in pathological hypertrophic hearts from humans and experimental animals. The reduction in Tom70 expression produced distinct pathological cardiomyocyte hypertrophy both in vivo and in vitro. The defective mitochondrial import of Tom70-targeted optic atrophy-1 triggered intracellular oxidative stress, which led to a pathological cellular response. Importantly, increased Tom70 levels provided cardiomyocytes with full resistance to diverse pro-hypertrophic insults. Together, these results reveal that Tom70 acts as a molecular switch that orchestrates hypertrophic stresses and mitochondrial responses to determine pathological cardiac hypertrophy.

Indexed as

AnimalsCardiomegalyDisease Models, AnimalDown-RegulationHeart FailureHumansMaleMiceMice, Inbred C57BLMitochondrial Membrane Transport ProteinsMitochondrial Precursor Protein Import Complex ProteinsMyocytes, CardiacOxidative StressRatsRats, Sprague-DawleyRNA InterferenceMitochondrial Membrane Transport ProteinsMitochondrial Precursor Protein Import Complex ProteinsRNA, Small InterferingTOMM70 protein, human

Identifiers

PMID25022898
PMCPMC4123302
OpenAlexW2065436048

What OpenQuestion 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 OpenQuestion graph.