Evidence map›Paper›PMID 35237363›Full record

ArticleWorld journal of emergency medicine2022

The expression of oxidative stress genes related to myocardial ischemia reperfusion injury in patients with ST-elevation myocardial infarction.

Qian-Lin Gu, Peng Jiang, Hui-Fen Ruan, Hao Tang, Yang-Bing Liang, Zhong-Fu Ma, Hong Zhan

Open access · bronzeAbstract read
In one paragraph

Article in World journal of emergency medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Myocardial injury caused byWorld journal of emergency medicine · 2024
    Article
  3. Article
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

7 authors at 2 institutions in 1 country.

Qian-Lin GuEmergency Department, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510000, China.
Peng JiangEmergency Department, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510000, China.
Hui-Fen RuanHuangpu District Emergency Department, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510000, China.
Hao TangEmergency Department, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510000, China.
Yang-Bing LiangEmergency Department, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510000, China.
Zhong-Fu MaEmergency Department, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510000, China.
Hong ZhanEmergency Department, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510000, China.
The First Affiliated Hospital, Sun Yat-sen University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWe aimed to investigate the gene expression of myocardial ischemia/reperfusion injury (MIRI) in patients with acute ST-elevation myocardial infarction (STEMI) using stress and toxicity pathway gene chip technology and try to determine the underlying mechanism.

methodsThe mononuclear cells were separated by ficoll centrifugation, and plasma total antioxidant capacity (T-AOC) was determined by the ferric reducing ability of plasma (FRAP) assay. The expression of toxic oxidative stress genes was determined and verified by oligo gene chip and quantitative real-time polymerase chain reaction (qRT-PCR). Additionally, gene ontology (GO) enrichment analysis was performed on DAVID website to analyze the potential mechanism further.

resultsThe total numbers of white blood cells (WBC) and neutrophils (N) in the peripheral blood of STEMI patients (the AMI group) were significantly higher than those in the control group (WBC: 11.67±4.85 ×10

conclusionsWBCs, especially neutrophils, were the critical cells that mediating reperfusion injury. MIRI was regulated by various genes, including oxidative metabolic stress, heat shock, DNA damage and repair, and apoptosis-related genes. The underlying pathway may be associated with UPR and apoptosis, which may be the novel therapeutic target.

Indexed as

Acute myocardial infarctionCYP1A1Myocardial ischemia/reperfusion injuryOxidative stressTNFSF6Unfolded protein response

Identifiers

PMID35237363
PMCPMC8861342
OpenAlexW3217212516

What OpenQuestion holds

Textmetadata
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.