Evidence map›Paper›PMID 33936386›Full record

ArticleOxidative medicine and cellular longevity2021

Rap1GAP Mediates Angiotensin II-Induced Cardiomyocyte Hypertrophy by Inhibiting Autophagy and Increasing Oxidative Stress.

Yan Gao, Di Zhao, Wen-Zhi Xie, Tingting Meng, Chunxiao Xu, Yutong Liu, Pengfei Zhang, Xiuping Bi, Zhuo Zhao

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

12 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. 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

9 authors at 2 institutions in 1 country.

Yan GaoDepartment of Cardiology, Jinan Central Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250014, China.ORCID https://orcid.org/0000-0003-4792-1109
Di ZhaoDepartment of Cardiology, The Third Affiliated Hospital of Shandong First Medical University (Affiliated Hospital of Shandong Academy of Medical Sciences), Jinan 250031, China.
Wen-Zhi XieDepartment of Cardiology, Jinan Central Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250014, China.
Tingting MengDepartment of Cardiology, Jinan Central Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250014, China.
Chunxiao XuDepartment of Cardiology, Jinan Central Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250014, China.
Yutong LiuDepartment of Cardiology, Jinan Central Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250014, China.
Pengfei ZhangDepartment of Cardiology, Jinan Central Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250014, China.
Xiuping BiDepartment of Cardiology, Jinan Central Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250014, China.
Zhuo ZhaoDepartment of Cardiology, Jinan Central Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250014, China.ORCID https://orcid.org/0000-0002-9671-6614
Shandong University · CNAffiliated Hospital of Shandong Academy of Medical Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal autophagy and oxidative stress contribute to angiotensin II- (Ang II-) induced cardiac hypertrophy and heart failure. We previously showed that Ang II increased Rap1GAP gene expression in cardiomyocytes associated with hypertrophy and autophagy disorders. Using real-time PCR and Western blot, we found that Rap1GAP expression was increased in the heart of Sprague Dawley (SD) rats infused by Ang II compared with saline infusion and in Ang II vs. vehicle-treated rat neonatal cardiomyocytes. Overexpression of Rap1GAP in cultured cardiomyocytes exacerbated Ang II-induced cardiomyocyte hypertrophy, reactive oxygen species (ROS) generation, and cell apoptosis and inhibited autophagy. The increased oxidative stress caused by Rap1GAP overexpression was inhibited by the treatment of autophagy agonists. Knockdown of Rap1GAP by siRNA markedly attenuated Ang II-induced cardiomyocyte hypertrophy and oxidative stress and enhanced autophagy. The AMPK/AKT/mTOR signaling pathway was inhibited by overexpression of Rap1GAP and activated by the knockdown of Rap1GAP. These results show that Rap1GAP-mediated pathway might be a new mechanism of Ang II-induced cardiomyocyte hypertrophy, which could be a potential target for the future treatment of cardiac hypertrophy and heart failure.

Indexed as

Angiotensin IIAnimalsAutophagyCardiomegalyGTPase-Activating ProteinsOxidative StressRatsRats, Sprague-DawleyRats, WistarAngiotensin IIGTPase-Activating ProteinsRap1GAP protein, mouse

Identifiers

PMID33936386
PMCPMC8062190
OpenAlexW3155474617

What OpenQuestion 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 OpenQuestion graph.