Evidence map›Paper›PMID 37129843›Full record

ArticleCell biochemistry and biophysics2023

PPARγ Regulates Macrophage Polarization by Inhibiting the JAK/STAT Pathway and Attenuates Myocardial Ischemia/Reperfusion Injury In Vivo.

Shengnan Wang, Yinlian Cai, Rongsheng Bu, Yaoguo Wang, Qingfan Lin, Youfang Chen, Chunchun Wu

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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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

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  10. Type 2 diabetes mellitus in adults: pathogenesis, prevention and therapy.Signal transduction and targeted therapy · 2024 · on this map
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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

7 authors at 3 institutions in 1 country.

Shengnan WangDepartment of Cardiology, the Second Affiliated Hospital of Fujian Medical University, Quanzhou City, 362000, Fujian, China.
Yinlian CaiDepartment of Cardiology, the Second Affiliated Hospital of Fujian Medical University, Quanzhou City, 362000, Fujian, China.
Rongsheng BuDepartment of Cardiology, the Second Affiliated Hospital of Fujian Medical University, Quanzhou City, 362000, Fujian, China.
Yaoguo WangDepartment of Cardiology, the Second Affiliated Hospital of Fujian Medical University, Quanzhou City, 362000, Fujian, China.
Qingfan LinDepartment of Clinical Medicine, Quanzhou Medical College, Quanzhou City, 362000, Fujian, China.
Youfang ChenDepartment of Clinical Medicine, Quanzhou Medical College, Quanzhou City, 362000, Fujian, China.
Chunchun WuDepartment of Cardiology, the Second Affiliated Hospital of Fujian Medical University, Quanzhou City, 362000, Fujian, China. wuchunchun@fjmu.edu.cn.
Fujian Medical University · CNQuanzhou Normal University · CNSecond Affiliated Hospital of Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study aimed to investigate the role of PPARγ and underlying mechanisms in myocardial ischemia/reperfusion injury (IRI). IRI was surgically induced in mice and neonatal rat cardiomyocytes (NRCM) were exposed to oxygen-glucose deprivation and reoxygenation (OGD/R). Quantitative genetic analysis and western blotting were performed to assess mRNA and protein levels, respectively, of PPARγ, as well as of different inflammatory, fibrosis, and apoptosis markers in cells and tissues. PPARγ was overexpressed in the heart of mice and NRCMs by viral transfection. Apoptosis and fibrosis were detected by TUNEL and Masson's trichrome staining, respectively. Enzyme-linked immunosorbent assay was performed to detect M1 and M2 macrophage-related inflammatory factors present in mouse sera. PPARγ overexpression significantly inhibited OGD/R- and IRI-induced cardiomyocyte apoptosis and fibrosis in vitro and in vivo. Moreover, PPARγ overexpression inhibited IRI-induced secretion of M1-related proinflammatory factors, whereas it supported the secretion of M2-related anti-inflammatory factors. Notably, these events were found to be mediated by the JAK/STAT pathway. In conclusion, PPARγ regulates macrophage polarization upon IRI via the JAK/STAT pathway, which will in turn prevent myocardial apoptosis and fibrosis. Hence, PPARγ may represent a valuable target for myocardial IRI treatment.

Indexed as

Myocardial Reperfusion InjuryReperfusion InjuryAnimalsApoptosisFibrosisGlucoseJanus KinasesMacrophagesPPAR gammaRatsSignal TransductionSTAT Transcription FactorsGlucoseJanus KinasesPPAR gammaSTAT Transcription FactorsJAK/STAT pathwayMyocardial apoptosisMyocardial fibrosisPolarized macrophagesPPARγ

Identifiers

PMID37129843
OpenAlexW4367668330

What Socratic 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 Socratic graph.