Evidence map›Paper›PMID 34581005›Full record

ArticleJournal of cellular and molecular medicine2021

Interleukin-7 aggravates myocardial ischaemia/reperfusion injury by regulating macrophage infiltration and polarization.

Mengwen Yan, Yaliu Yang, Ying Zhou, Changan Yu, Rui Li, Wei Gong, Jingang Zheng

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

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  12. hESC-Derived Epicardial Cells Promote Repair of Infarcted Hearts in Mouse and Swine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  13. Communications between macrophages and cardiomyocytes.Cell communication and signaling : CCS · 2023
    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

7 authors at 4 institutions in 1 country.

Mengwen YanDepartment of Cardiology, China-Japan Friendship Hospital, Beijing, China.
Yaliu YangDepartment of Cardiology, China-Japan Friendship Hospital, Beijing, China.
Ying ZhouDepartment of Cardiology, China-Japan Friendship Hospital, Beijing, China.
Changan YuCentral Laboratory of Cardiovascular Disease, China-Japan Friendship Hospital, Beijing, China.
Rui LiDepartment of Health Care, China-Japan Freindship Hospital, Ministry of Health, Beijing, China.
Wei GongEmergency and Critical Care Center, Beijing Anzhen Hospital Capital Medical University, Beijing, China.ORCID 0000-0002-3298-7001
Jingang ZhengDepartment of Cardiology, China-Japan Friendship Hospital, Beijing, China.
China-Japan Friendship Hospital · CNBeijing Hospital · CNCapital Medical University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin (IL)-7 is known to enhance the macrophages cytotoxic activity and that macrophages play a pivotal role in the development and progression of myocardial ischaemia/reperfusion (I/R) injury. However, the effects of IL-7 on macrophages infiltration and polarization in myocardial I/R injury are currently unclear. This study aimed to evaluate the effects of the IL-7 expression on myocardial I/R injury and their relationship with macrophages. The data showed that IL-7 expression in mouse heart tissue increases following I/R injury and that IL-7 knockout or anti-IL-7 antibody treatment significantly improve I/R injury, including reduction in myocardial infarction area, a serum troponin T level decreases and an improvement in cardiac function. On the other hand, recombinant IL-7 (rIL-7) supplementation induces opposite effects and the anti-IL-7 antibody significantly reduces the cardiomyocyte apoptosis and macrophage infiltration. rIL-7 cannot directly cause apoptosis, but it can induce cardiomyocyte apoptosis through macrophages, in addition to increase the macrophages migration in vitro. Anti-IL-7 antibody affects the cytokine production in T helper (Th) 1 and Th2 cells and also promotes the macrophages differentiation to M2 macrophages. However, anti-IL-7 antibody does not reduce the M1 macrophage number, and it only increases the ratio of M2/M1 macrophages in mice heart tissues after I/R injury. Taking together, these data reveal that IL-7 plays an intensifying role in myocardial I/R injury by promoting cardiomyocyte apoptosis through the regulation of macrophage infiltration and polarization.

Indexed as

AnimalsApoptosisBiomarkersDisease Models, AnimalDisease SusceptibilityGene ExpressionHeart Function TestsHemodynamicsImmunophenotypingInterleukin-7Macrophage ActivationMacrophagesMiceMice, KnockoutMyocardial Reperfusion InjuryMyocytes, CardiacBiomarkersInterleukin-7interleukin-7ischaemia/reperfusion injurymacrophagemyocardial

Identifiers

PMID34581005
PMCPMC8572772
OpenAlexW3204303112

What OpenQuestion holds

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LicenceCC BY
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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.