Evidence mapPaperPMID 33246164Full record

ArticleJournal of sport and health science2021

Dynamic resistance exercise increases skeletal muscle-derived FSTL1 inducing cardiac angiogenesis via DIP2A-Smad2/3 in rats following myocardial infarction.

Yue Xi, Meili Hao, Qiaoqin Liang, Yongxia Li, Da-Wei Gong, Zhenjun Tian

Open access · diamondAbstract read
In one paragraph

Article in Journal of sport and health science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 4 pooled it
2.9field-weighted citation impact, top 8% 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

46 citing papers in PubMed, 4 syntheses or guidelines pooled it, 84 citations in OpenAlex.

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  16. Exercise intensity and cardiac metabolic adaptations in elderly heart failure rehabilitation: A review.International journal of cardiology. Cardiovascular risk and prevention · 2025
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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 2 institutions in 2 countries.

Yue XiInstitute of Sports and Exercise Biology, Shaanxi Normal University, Xi'an 710119, China.
Meili HaoInstitute of Sports and Exercise Biology, Shaanxi Normal University, Xi'an 710119, China; School of Physical Education, Luoyang Normal University, Luoyang 471934, China.
Qiaoqin LiangInstitute of Sports and Exercise Biology, Shaanxi Normal University, Xi'an 710119, China.
Yongxia LiSchool of Life Science, Shaanxi Normal University, Xi'an 710119, China.
Da-Wei GongDivision of Endocrinology, Diabetes and Nutrition, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Zhenjun TianInstitute of Sports and Exercise Biology, Shaanxi Normal University, Xi'an 710119, China. Electronic address: tianzj2013@hotmail.com.
Shaanxi Normal University · CNUniversity of Maryland, Baltimore · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe aim of this study was to investigate the potential of dynamic resistance exercise to generate skeletal muscle-derived follistatin like-1 (FSTL1), which may induce cardioprotection in rats following myocardial infarction (MI) by inducing angiogenesis.

methodsMale, adult Sprague-Dawley rats were randomly divided into 5 groups (n = 12 in each group): sham group (S), sedentary MI group (MI), MI + resistance exercise group (MR), MI + adeno-associated virus (AAV)-FSTL1 injection group (MA), and MI + AAV-FSTL1 injection + resistance exercise group (MAR). The AAV-FSTL1 vector was prepared by molecular biology methods and injected into the anterior tibialis muscle. The MI model was established by ligation of the left anterior descending coronary artery. Rats in the MR and MAR groups underwent 4 weeks of dynamic resistance exercise training using a weighted climbing-up ladder. Heart function was evaluated by hemodynamic measures. Collagen volume fraction of myocardium was observed and analyzed by Masson's staining. Human umbilical vein vessel endothelial cells culture and recombinant human FSTL1 protein or transforming growth factor-β receptor 1 (TGFβR1) inhibitor treatment were used to elucidate the molecular signaling mechanism of FSTL1. Angiogenesis, cell proliferation, and disco interacting protein 2 homolog A (DIP2A) location were observed by immunofluorescence staining. The expression of FSTL1, DIP2A, and the activation of signaling pathways were detected by Western blotting. Angiogenesis of endothelial cells was observed by tubule experiment. One-way analysis of variance and Student's t test were used for statistical analysis.

resultsResistance exercise stimulated the secretion of skeletal muscle FSTL1, which promoted myocardial angiogenesis, inhibited pathological remodeling, and protected cardiac function in MI rats. Exercise facilitated skeletal muscle FSTL1 to play a role in protecting the heart. Exogenous FSTL1 promoted the human umbilical vein vessel endothelial cells proliferation and up-regulated the expression of DIP2A, while TGFβR1 inhibitor intervention down-regulated the phosphorylation level of Smad2/3 and the expression of vascular endothelial growth factor-A, which was not conducive to angiogenesis. FSTL1 bound to the receptor, DIP2A, to regulate angiogenesis mainly through the Smad2/3 signaling pathway. FSTL1-DIP2A directly activated Smad2/3 and was not affected by TGFβR1.

conclusionDynamic resistance exercise stimulates the expression of skeletal muscle-derived FSTL1, which could supplement the insufficiency of cardiac FSTL1 and promote cardiac rehabilitation through the DIP2A-Smad2/3 signaling pathway in MI rats.

Indexed as

Angiogenesis Inducing AgentsAnimalsDisease Models, AnimalFollistatin-Related ProteinsMaleMuscle, SkeletalMyocardial InfarctionNuclear ProteinsPhysical Conditioning, AnimalRatsRats, Sprague-DawleySmad2 ProteinSmad3 ProteinUp-RegulationAngiogenesis Inducing AgentsFollistatin-Related ProteinsFstl1 protein, ratNuclear ProteinsSmad2 ProteinSmad2 protein, ratSmad3 ProteinSmad3 protein, ratAngiogenesisFollistatin like-1Myocardial infarctionResistance exerciseSignaling mechanism

Identifiers

PMID33246164
PMCPMC8500809
OpenAlexW3107038321

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.