Evidence map›Paper›PMID 34460026›Full record

ArticleInflammation2022

SHP-1/STAT3 Interaction Is Related to Luteolin-Induced Myocardial Ischemia Protection.

Donghai Liu, Hong Luo, Chenhui Qiao

Open access · bronzeAbstract read
In one paragraph

Article in Inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. LILRB4 Recruits SHP-1 to Enhance Oxidative Stress and Apoptosis, Aggravating Myocardial Ischemia-Reperfusion Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  18. Immunopharmacological Activities of Luteolin in Chronic Diseases.International journal of molecular sciences · 2023
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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

3 authors at 1 institution in 1 country.

Donghai LiuCardiovascular Surgery II, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Hong LuoCardiovascular Surgery II, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Chenhui QiaoCardiovascular Surgery II, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China. qchenhui@yeah.net.ORCID http://orcid.org/0000-0002-2599-3198
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prevention and management of myocardial ischemia/reperfusion (I/R) injury is a key step in coronary heart disease surgery. Luteolin is a falconoid compound that has an antioxidant effect, but its mechanism in I/R injury in vivo and in vitro is still under explored. This study attempted to reveal the role of luteolin (Lut) in I/R through mediation of the Src homology 2 domain-containing protein tyrosine phosphatase 1 (SHP-1)/Signal transducer and activator of transcription 3 (STAT3) pathway. To establish I/R rat models, the left anterior descending artery (LAD) was ligated for 30 min and re-perfused for 1 h in Lut-pretreated or nude rats. Comparisons between infarct area, cardiac dysfunction, and myocardial cell death and inflammatory reaction were performed in I/R-induced rats. Hypoxia/reoxygenation (H/R) cell models were established by stimulating H9c2 cells with 95% nitrogen and 5% carbon dioxide. Simultaneously, H/R-related cell death and inflammatory reactions were investigated following Lut treatment. The target protein of Lut was identified using western blotting. Pro-inflammatory cytokines were also measured in serum or Lut-pretreated cell culture medium. The results revealed that compared with the I/R group, Lut treatment could significantly decrease myocardial infarction (MI) area, increase left ventricular ejection fraction (LVEF), and decrease cell death and pro-inflammatory cytokines in the serum. Decreased apoptosis and inflammatory cytokines were also observed in H/R cells after Lut treatment. Lut treatment downregulated SHP-1 expression and subsequently upregulated STAT3 phosphorylation in both I/R rat heart tissue and H9c2 cells. The findings of the current study suggest that Lut can protect the heart and reduce MI area, cell apoptosis rate, and inflammatory level in I/R models.

Indexed as

AnimalsApoptosisBiomarkersCardiotonic AgentsDown-RegulationLuteolinMaleMyocardial Reperfusion InjuryProtein Tyrosine Phosphatase, Non-Receptor Type 6Random AllocationRatsRats, Sprague-DawleySTAT3 Transcription FactorTreatment OutcomeUp-RegulationBiomarkersCardiotonic AgentsLuteolinProtein Tyrosine Phosphatase, Non-Receptor Type 6Ptpn6 protein, ratStat3 protein, ratSTAT3 Transcription FactorHypoxia/Reoxygenation Injury;Ischemia/Reperfusion Injury;Luteolin;Myocardial Ischemia;SHP-1;STAT3.

Identifiers

PMID34460026
PMCPMC8403691
OpenAlexW3196825958

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.