Evidence map›Paper›PMID 31930683›Full record

ArticleJournal of cellular and molecular medicine2020

Heat shock transcription factor 1 regulates exercise-induced myocardial angiogenesis after pressure overload via HIF-1α/VEGF pathway.

Xu Tian, Ning Zhou, Jie Yuan, Le Lu, Qi Zhang, Minmin Wei, Yunzeng Zou, Lingyan Yuan

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
1.5field-weighted citation impact, top 18% 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, 2 syntheses or guidelines pooled it, 33 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Xu TianDepartment of Kinesiology, Institute of Physical Education, Shanghai Normal University, Shanghai, China.ORCID 0000-0003-0110-2140
Ning ZhouSection of Cardiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jie YuanShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biological Science, Fudan University, Shanghai, China.
Le LuDepartment of Kinesiology, Institute of Physical Education, Shanghai Normal University, Shanghai, China.
Qi ZhangDepartment of Kinesiology, Institute of Physical Education, Shanghai Normal University, Shanghai, China.
Minmin WeiDepartment of Kinesiology, Institute of Physical Education, Shanghai Normal University, Shanghai, China.
Yunzeng ZouShanghai Institute of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biological Science, Fudan University, Shanghai, China.
Lingyan YuanDepartment of Kinesiology, Institute of Physical Education, Shanghai Normal University, Shanghai, China.
Shanghai Normal University · CNSun Yat-sen University · CNTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exercise training is believed to have a positive effect on cardiac hypertrophy after hypertension. However, its mechanism is still not fully understood. Herein, our findings suggest that heat shock transcription factor 1 (HSF1) improves exercise-initiated myocardial angiogenesis after pressure overload. A sustained narrowing of the diagonal aorta (TAC) and moderately- intense exercise training protocol were imposed on HSF1 heterozygote (KO) and their littermate wild-type (WT) male mice. After two months, the cardiac function was assessed using the adaptive responses to exercise training, or TAC, or both of them such as catheterization and echocardiography. The HE stains assessed the area of myocyte cross-sectional. The Western blot and real-time PCR measured the levels of expression for heat shock factor 1 (HSF1), vascular endothelial growth factor (VEGF) and hypoxia inducible factor-1 alpha (HIF-1α) in cardiac tissues. The anti-CD31 antibody immunohistochemical staining was done to examine how exercise training influenced cardiac ontogeny. The outcome illustrated that exercise training significantly improved the cardiac ontogeny in TAC mice, which was convoyed by elevated levels of expression for VEGF and HIF-1α and preserved the heart microvascular density. More importantly, HSF1 deficiency impaired these effects induced by exercise training in TAC mice. In conclusion, exercise training encourages cardiac ontogeny by means of HSF1 activation and successive HIF-1α/VEGF up-regulation in endothelial cells during continued pressure overload.

Indexed as

AnimalsAortaCardiomegalyCross-Sectional StudiesEndothelial CellsHeat Shock Transcription FactorsHypoxia-Inducible Factor 1, alpha SubunitMaleMiceMice, Inbred C57BLMyocardiumMyocytes, CardiacNeovascularization, PathologicUp-RegulationVascular Endothelial Growth Factor AHeat Shock Transcription FactorsHif1a protein, mouseHsf1 protein, mouseHypoxia-Inducible Factor 1, alpha SubunitVascular Endothelial Growth Factor Avascular endothelial growth factor A, mousecardiac angiogenesisexercise trainingHSF1pressure overload

Identifiers

PMID31930683
PMCPMC7011135
OpenAlexW2998834580

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.