Evidence map›Paper›PMID 36374849›Full record

ArticleJournal of sport and health science2023

Exercise training attenuates angiotensin II-induced cardiac fibrosis by reducing POU2F1 expression.

Na Feng, Haiyi Yu, Yueshen Wang, Youyi Zhang, Han Xiao, Wei Gao

Open access · diamondAbstract read
In one paragraph

Article in Journal of sport and health science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Exercise inhibits proliferation and induces apoptosis of lung adenocarcinoma cells via the POU2F2-SPOCD1-PI3K/AKT signaling axis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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 4 institutions in 2 countries.

Na FengDepartment of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing 100191, China.
Haiyi YuDepartment of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing 100191, China.
Yueshen WangDepartment of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing 100191, China.
Youyi ZhangDepartment of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing 100191, China; Research Unit of Medical Science Research Management/Basic and Clinical Research of Metabolic Cardiovascular Diseases, Chinese Academy of Medical Sciences, Beijing 100191, China.
Han XiaoDepartment of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing 100191, China; Research Unit of Medical Science Research Management/Basic and Clinical Research of Metabolic Cardiovascular Diseases, Chinese Academy of Medical Sciences, Beijing 100191, China. Electronic address: xiaohan@bjmu.edu.cn.
Wei GaoDepartment of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing 100191, China. Electronic address: weigao@bjmu.edu.cn.
Ministry of Education · ROPeking University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNPeking University Third Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExercise training protects against heart failure. However, the mechanism underlying the protective effect of exercise training on angiotensin II (Ang II)-induced cardiac fibrosis remains unclear.

methodsAn exercise model involving C57BL/6N mice and 6 weeks of treadmill training was used. Ang II (1.44 mg/kg/day) was administered to induce cardiac fibrosis. RNA sequencing and bioinformatic analysis were used to identify the key factors mediating the effects of exercise training on cardiac fibrosis. Primary adult mouse cardiac fibroblasts (CFs) were used in vitro. Adeno-associated virus serotype 9 was used to overexpress POU domain, class 2, transcription factor 1 (POU2F1) in vivo.

resultsExercise training attenuated Ang II-induced cardiac fibrosis and reversed 39 gene expression changes. The transcription factor regulating the largest number of these genes was POU2F1. Compared to controls, POU2F1 was shown to be significantly upregulated by Ang II, which is itself reduced by exercise training. In vivo, POU2F1 overexpression nullified the benefits of exercise training on cardiac fibrosis. In CFs, POU2F1 promoted cardiac fibrosis. CCAAT enhancer-binding protein β (C/EBPβ) was predicted to be the transcription factor of POU2F1 and verified using a dual-luciferase reporter assay. In vivo, exercise training activated AMP-activated protein kinase (AMPK) and alleviated the increase in C/EBPβ induced by Ang II. In CFs, AMPK agonist inhibited the increase in C/EBPβ and POU2F1 induced by Ang II, whereas AMPK inhibitor reversed this effect.

conclusionExercise training attenuates Ang II-induced cardiac fibrosis by reducing POU2F1. Exercise training inhibits POU2F1 by activating AMPK, which is followed by the downregulation of C/EBPβ, the transcription factor of POU2F1.

Indexed as

AMP-Activated Protein KinasesMyocardiumAngiotensin IIAnimalsFibrosisMiceMice, Inbred C57BLTranscription FactorsAMP-Activated Protein KinasesAngiotensin IITranscription FactorsAMPKCardiac fibrosisC/EBPβExercisePOU2F1

Identifiers

PMID36374849
PMCPMC10362488
OpenAlexW4307814011

What Socratic 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 Socratic graph.