Evidence map›Paper›PMID 34550233›Full record

ArticleArquivos brasileiros de cardiologia2021

VEGF121 Mediates Post-Hypoxia Cardioprotective Effects Via CaSR and Mitochondria-Dependent Protease Pathway.

Yan Zhang, Wei-Hua Yin, Fan Yang, Yun-Qiang An, Wei Zhou, Hui Yu, Hong Xie, Yan-Ling Zhang, Yue Zhu, Xiang-Chun Shen and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Arquivos brasileiros de cardiologia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 47% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Low molecular weight hyaluronan inhibits lung epithelial ion channels by activating the calcium-sensing receptor.Matrix biology : journal of the International Society for Matrix Biology · 2023
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  3. Review
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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

11 authors at 3 institutions in 1 country.

Yan ZhangHospital of Guizhou Medical University, Guiyang - China.
Wei-Hua YinChinese Academy of Medical Sciences and Peking Union Medical College, Beijing - China.
Fan YangHospital of Guizhou Medical University, Guiyang - China.
Yun-Qiang AnChinese Academy of Medical Sciences and Peking Union Medical College, Beijing - China.
Wei ZhouHospital of Guizhou Medical University, Guiyang - China.
Hui YuHospital of Guizhou Medical University, Guiyang - China.
Hong XieHospital of Guizhou Medical University, Guiyang - China.
Yan-Ling ZhangHospital of Guizhou Medical University, Guiyang - China.
Yue ZhuHospital of Guizhou Medical University, Guiyang - China.
Xiang-Chun ShenHospital of Guizhou Medical University, Guiyang - China.
Ruiqing TianThe First People's Hospital of Guiyang, Guiyang - China.ORCID 0000-0001-5076-9844
Guiyang Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNThe First People's Hospital of Guiyang · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiovascular disease is the major cause of death worldwide. Hypoxia-mediated apoptosis in cardiomyocytes is a major cause of cardiovascular disorders. Treatment with vascular endothelial growth factor (VEGF) protein has been tested but operational difficulties have limited its use. However, with the advancements of gene therapy, interest has risen in VEGF-based gene therapy in cardiovascular disorders. However, the precise mechanism by which VEGF replenishment rescues post-hypoxia damage in cardiomyocytes is not known.

objectivesTo investigate the effect of post-hypoxia VEGF121 expression using neonatal rat cardiomyocytes.

methodsCardiomyocytes isolated from neonatal rats were used to establish an in vitro model of hypoxia-induced cardiac injury. The effect of VEGF overexpression, alone or in combination with small-molecule inhibitors targeting calcium channel, calcium sensitive receptors (CaSR), and calpain on cell growth and proliferation on hypoxia-induced cardiomyocyte injury were determined using an MTT assay, TUNEL staining, Annexin V/PI staining, lactate dehydrogenase and caspase activity. For statistical analysis, a value of P<0.05 was considered to be significant.

resultsThe effect of VEGF121 was found to be mediated by CaSR and calpain but was not dependent on calcium channels.

conclusionsOur findings, even though using an in vitro setting, lay the foundation for future validation and pre-clinical testing of VEGF-based gene therapy in cardiovascular diseases.

Indexed as

Receptors, Calcium-SensingVascular Endothelial Growth Factor AAnimalsHypoxiaMitochondriaMyocytes, CardiacPeptide HydrolasesRatsPeptide HydrolasesReceptors, Calcium-SensingVascular Endothelial Growth Factor A

Identifiers

PMID34550233
PMCPMC8462959
OpenAlexW3196339084

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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.