Evidence map›Paper›PMID 35996142›Full record

ArticleBiology direct2022

Downregulation of amphiregulin improves cardiac hypertrophy via attenuating oxidative stress and apoptosis.

Mingyue Ji, Yun Liu, Zhi Zuo, Cheng Xu, Li Lin, Yong Li

Open access · goldAbstract read
In one paragraph

Article in Biology direct, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

18 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Amphiregulin and Fibrosis: Existing Evidence and Future Directions.International journal of molecular sciences · 2025
    Review
  8. Amphiregulin in Fibrotic Diseases and Cancer.International journal of molecular sciences · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Annals of medicine · 2024
    Article
  15. [Therapeutic Effect of Cang-Ai Volatile Oil on High-Altitude Rats With Cardiac Hypertrophy Through Modulation of Oxidative Stress Response].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024
    Article
  16. Review
  17. Article
  18. 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

6 authors at 3 institutions in 1 country.

Mingyue Ji *Department of Cardiology, Lianshui County People's Hospital, Huaian, China.
Yun Liu *Department of Intensive Care Medicine, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zhi ZuoDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China.
Cheng XuDepartment of Cardiology, Lianshui County People's Hospital, Huaian, China.
Li LinDepartment of Cardiovascular Medicine, East Hospital, Tongji University School of Medicine, 150 JimoRoad, Shanghai, 200120, China. linli777@126.com.
Yong LiDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029, Jiangsu Province, China. liyongmydream@126.com.
Nanjing Medical University · CNJiangsu Province Hospital · CNShanghai East Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amphiregulin (AREG) is a ligand of epidermal growth factor receptor and participates in the fibrosis of multiple organs. However, whether AREG can regulate hypertrophic cardiomyopathy is not well known. This research aims to explore the effect of AREG on cardiac hypertrophy, and whether the oxidative stress and apoptosis was involved in the influence of AREG on cardiac hypertrophy. Angiotensin (Ang) II induced cardiac hypertrophy in mice and neonatal rat cardiomyocytes (NRCMs) or HL-1 cells in vitro. AREG expressions raised in the heart of mice. After AREG downregulation, the increases of Ang II induced cardiac weight and cardiomyocytes area were inhibited. Down-regulation of AREG could inhibit Ang II induced the increases of atrial natriuretic peptide, brain natriuretic peptide, beta-myosin heavy chain in the heart of mice, and NRCMs and HL-1 cells. The enhancement of oxidative stress in mice heart with Ang II treatment was alleviated by AREG knockdown. The raises of Ang II induced Bax and cleaved caspase3 in mice heart were inhibited by AREG downregulation. AREG downregulation reduced myocardial hypertrophy via inhibition of oxidative and apoptosis. AREG may be a target for future cardiac hypertrophy treatment.

Indexed as

AmphiregulinApoptosisCardiomegalyOxidative StressAngiotensin IIAnimalsDown-RegulationMiceRatsAmphiregulinAngiotensin IIAreg protein, mouseAreg protein, ratAmphiregulinApoptosisCardiac hypertrophyOxidative stress

Identifiers

PMID35996142
PMCPMC9394079
OpenAlexW4292566698

What Socratic holds

Textmetadata
LicenceCC BY
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.