Evidence map›Paper›PMID 36386478›Full record

ArticleActa pharmaceutica Sinica. B2022

Cardiac fibroblast heat shock protein 47 aggravates cardiac fibrosis post myocardial ischemia-reperfusion injury by encouraging ubiquitin specific peptidase 10 dependent Smad4 deubiquitination.

Saiyang Xie, Yun Xing, Wenke Shi, Min Zhang, Mengya Chen, Wenxi Fang, Shiqiang Liu, Tong Zhang, Xiaofeng Zeng, Si Chen and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Acta pharmaceutica Sinica. B, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Journal of the American Heart Association · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025
    Review
  13. Article
  14. Article
  15. Ubiquitin proteasome system in cardiac fibrosis.Journal of advanced research · 2025
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

13 authors at 1 institution in 1 country.

Saiyang XieDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Yun XingDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Wenke ShiDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Min ZhangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Mengya ChenDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Wenxi FangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Shiqiang LiuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Tong ZhangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Xiaofeng ZengCardiovascular Research Institute of Wuhan University, Wuhan 430060, China.
Si ChenCardiovascular Research Institute of Wuhan University, Wuhan 430060, China.
Shasha WangCardiovascular Research Institute of Wuhan University, Wuhan 430060, China.
Wei DengDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Qizhu TangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite complications were significantly reduced due to the popularity of percutaneous coronary intervention (PCI) in clinical trials, reperfusion injury and chronic cardiac remodeling significantly contribute to poor prognosis and rehabilitation in AMI patients. We revealed the effects of HSP47 on myocardial ischemia-reperfusion injury (IRI) and shed light on the underlying molecular mechanism. We generated adult mice with lentivirus-mediated or miRNA (mi1/133TS)-aided cardiac fibroblast-selective HSP47 overexpression. Myocardial IRI was induced by 45-min occlusion of the left anterior descending (LAD) artery followed by 24 h reperfusion in mice, while ischemia-mediated cardiac remodeling was induced by four weeks of reperfusion. Also, the role of HSP47 in fibrogenesis was evaluated in cardiac fibroblasts following hypoxia-reoxygenation (HR). Extensive HSP47 was observed in murine infarcted hearts, human ischemic hearts, and cardiac fibroblasts and accelerated oxidative stress and apoptosis after myocardial IRI. Cardiac fibroblast-selective HSP47 overexpression exacerbated cardiac dysfunction caused by chronic myocardial IRI and presented deteriorative fibrosis and cell proliferation. HSP47 upregulation in cardiac fibroblasts promoted TGF

Indexed as

Cardiac dysfunctionCardiac fibrosisCell proliferationFibroblastHeat shock protein 47Myocardial ischemia–reperfusion injurySmad4Ubiquitin-specific protease 10

Identifiers

PMID36386478
PMCPMC9643299
OpenAlexW4289943207

What OpenQuestion 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 OpenQuestion graph.