Evidence map›Paper›PMID 35861038›Full record

ArticleJournal of cellular and molecular medicine2022

Pirfenidone alleviates cardiac fibrosis induced by pressure overload via inhibiting TGF-β1/Smad3 signalling pathway.

Na Li, Weijian Hang, Hongyang Shu, Ning Zhou

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Cardiac fibrosis: from mechanisms and models to medicines.Trends in pharmacological sciences · 2025
    Review
  12. Review
  13. Cardioprotective Role of Captopril: From Basic to Applied Investigations.International journal of molecular sciences · 2025
    Review
  14. Article
  15. Review
  16. Biomolecules & biomedicine · 2024
    Article
  17. Article
  18. Pirfenidone use in fibrotic diseases: What do we know so far?Immunity, inflammation and disease · 2024
    Review
  19. Review
  20. 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

4 authors at 1 institution in 1 country.

Na LiDivision of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0000-0002-5724-4036
Weijian HangDivision of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Hongyang ShuDivision of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0000-0001-6808-8924
Ning ZhouDivision of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Tongji Hospital · CN

Funding

Chinese Cardiovascular Association-Access Fund 2020-CCA-ACCESS-059National Natural Science Foundation of China 81570261National Natural Science Foundation of China 82070316
6 · The paper itself

Abstract

Cardiac fibrosis critically injured the cardiac structure and function of the hypertensive patients. However, the anti-fibrotic strategy is still far from satisfaction. This study aims to determine the effect and mechanism of Pirfenidone (PFD), an anti-lung fibrosis medicine, in the treatment of cardiac fibrosis and heart failure induced by pressure overload. Male C57BL/6 mice were subjected to thoracic aorta constriction (TAC) or sham surgery with the vehicle, PFD (300 mg/kg/day) or Captopril (CAP, 20 mg/kg/day). After 8 weeks of surgery, mice were tested by echocardiography, and then sacrificed followed by morphological and molecular biological analysis. Compared to the sham mice, TAC mice showed a remarkable cardiac hypertrophy, interstitial and perivascular fibrosis and resultant heart failure, which were reversed by PFD and CAP significantly. The enhanced cardiac expression of TGF-β1 and phosphorylation of Smad3 in TAC mice were both restrained by PFD. Cardiac fibroblasts isolated from adult C57BL/6 mice were treated by Angiotensin II, which led to significant increases in cellular proliferation and levels of α-SMA, vimentin, TGF-β1 and phosphorylated TGF-β receptor and Smad3. These changes were markedly inhibited by pre-treatment of PFD. Collectively, PFD attenuates myocardial fibrosis and dysfunction induced by pressure overload via inhibiting the activation of TGF-β1/Smad3 signalling pathway.

Indexed as

Heart FailureTransforming Growth Factor beta1AnimalsFibrosisMaleMiceMice, Inbred C57BLMyocardiumPyridonesSmad3 ProteinpirfenidonePyridonesSmad3 ProteinTransforming Growth Factor beta1cardiac fibrosiscardiac remodellingpirfenidonepressure overloadtransforming growth factor-β1

Identifiers

PMID35861038
PMCPMC9357610
OpenAlexW4286007524

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.