Evidence map›Paper›PMID 37572219›Full record

ArticleCell biochemistry and biophysics2023

The Effect and Mechanism of POSTN and Its Alternative Splicing on the Apoptosis of Myocardial Cells in Acute Myocardial Infarction: A Study in Vitro.

Xuemei Liu, Zulikaier Tuerxusssn, Yumaierjiang Balati, Pengfei Gong, Ze Zhang, Zhen Bao, Yuchun Yang, Pengyi He, Muhuyati

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

Article in Cell biochemistry and biophysics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
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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

9 authors at 2 institutions in 1 country.

Xuemei LiuDepartment of Respiratory Medicine, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China.
Zulikaier TuerxusssnThe Second Department of Coronary Heart Disease, the First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China.
Yumaierjiang BalatiThe Second Department of Coronary Heart Disease, the First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China.
Pengfei GongDepartment of Integrated Cardiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China.
Ze ZhangThe Second Department of Coronary Heart Disease, the First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China.
Zhen BaoDepartment of Integrated Cardiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China.
Yuchun YangDepartment of Integrated Cardiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China.
Pengyi HeThe Second Department of Coronary Heart Disease, the First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China. 813058823@qq.com.
MuhuyatiDepartment of Integrated Cardiology, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, China. mhyt567@163.com.
Xinjiang Medical University · CNFirst Affiliated Hospital of Xinjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our study aimed to investigate key molecular targets in the pathogenesis of AMI, and provide new strategy for the treatment. In this work, the myocardial ischemia and hypoxia model was constructed by using HL-1 mouse cardiomyocytes. The over-expressing POSTN wild-type, mutant and negative control lentiviruses (GV492-POSTNWT,GV492-POSTN-MUT, GV492-NC) was conducted and transfected. Cardiomyocytes were examined for cell proliferation and apoptosis to explore the effects of POSTN and its alternative splicing. The endoplasmic reticulum stess-related apoptosis proteins were selected and detected. We found that POSTN could promote the proliferation of normal and hypoxic cardiomyocytes and inhibit their apoptosis. The mechanism by which POSTN inhibited cardiomyocyte apoptosis may be through inhibiting the GRP78-eIF2α-ATF4-CHOP pathway of endoplasmic reticulum stress. Alternative splicing of POSTN could inhibit the apoptosis of ischemic and hypoxic cardiomyocytes, and its mechanism needs to be confirmed by further studies. We drawed the conclusion that POSTN might be a potential therapeutic target for AMI.

Indexed as

Alternative SplicingCell Adhesion MoleculesMyocardial InfarctionMyocytes, CardiacAnimalsApoptosisApoptosis Regulatory ProteinsEndoplasmic Reticulum StressMiceApoptosis Regulatory ProteinsCell Adhesion MoleculesPostn protein, mouseAcute myocardial infarctionAlternative splicingApoptosisPOSTN

Identifiers

PMID37572219
PMCPMC10465634
OpenAlexW4385773909

What OpenQuestion holds

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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.