Evidence map›Paper›PMID 30858476›Full record

ArticleActa pharmacologica Sinica2019

Temporal dynamics of immune response following prolonged myocardial ischemia/reperfusion with and without cyclosporine A.

Vitali Rusinkevich, Yin Huang, Zhong-Yan Chen, Wu Qiang, Yi-Gang Wang, Yu-Fang Shi, Huang-Tian Yang

Open access · hybridAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 47 citations in OpenAlex.

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  12. Injury-induced myosin-specific tissue-resident memory T cells drive immune checkpoint inhibitor myocarditis.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  14. The Technique of Permanent Pericardial Catheter in Mice.JACC. Basic to translational science · 2024
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  17. CD47 blockade enhances phagocytosis of cardiac cell debris by neutrophils.International journal of cardiology. Heart & vasculature · 2023
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  19. hESC-Derived Epicardial Cells Promote Repair of Infarcted Hearts in Mouse and Swine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 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

7 authors at 3 institutions in 2 countries.

Vitali RusinkevichCAS Key Laboratory of Tissue Microenvironment and Tumor, Laboratory of Molecular Cardiology, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Yin HuangCAS Key Laboratory of Tissue Microenvironment and Tumor, Laboratory of Tumor and Stem Cell, Shanghai Institute of Nutrition and Health, SIBS, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Zhong-Yan ChenCAS Key Laboratory of Tissue Microenvironment and Tumor, Laboratory of Molecular Cardiology, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Wu QiangCAS Key Laboratory of Tissue Microenvironment and Tumor, Laboratory of Molecular Cardiology, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Yi-Gang WangDepartment of Pathology and Laboratory Medicine, College of Medicine, University of Cincinnati Medical Center, Cincinnati, OH, 45267, USA.
Yu-Fang ShiCAS Key Laboratory of Tissue Microenvironment and Tumor, Laboratory of Tumor and Stem Cell, Shanghai Institute of Nutrition and Health, SIBS, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Huang-Tian YangCAS Key Laboratory of Tissue Microenvironment and Tumor, Laboratory of Molecular Cardiology, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China. htyang@sibs.ac.cn.
Shanghai Institutes for Biological Sciences · CNUniversity of Chinese Academy of Sciences · CNUniversity of Cincinnati Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Understanding the dynamics of the immune response following late myocardial reperfusion is critical for the development of immunomodulatory therapy for myocardial infarction (MI). Cyclosporine A (CSA) possesses multiple therapeutic applications for MI, but its effects on the inflammation caused by acute MI are not clear. This study aimed to determine the dynamics of the immune response following myocardial ischemia/reperfusion (I/R) and the effects of CSA in a mouse model of prolonged myocardial ischemia designated to represent the human condition of late reperfusion. Adult C57BL/6 mice were subjected to 90 min of closed-chest myocardial I/R, which induced severe myocardial injury and excessive inflammation in the heart. Multicomponent analysis of the immune response caused by prolonged I/R revealed that the peak of cytokines/chemokines in the systemic circulation was synchronized with the maximal influx of neutrophils and T-cells in the heart 1 day after MI. The peak of cytokine/chemokine secretion in the infarcted heart coincided with the maximal macrophage and natural killer cell infiltration on day 3 after MI. The cellular composition of the mediastinal lymph nodes changed similarly to that of the infarcted hearts. CSA (10 mg/kg/day) given after prolonged I/R impaired heart function, enlarged the resulting scar, and reduced heart vascularization. It did not change the content of immune cells in hearts exposed to prolonged I/R, but the levels of MCP-1 and MIP-1α (hearts) and IL-12 (hearts and serum) were significantly reduced in the CSA-treated group in comparison to the untreated group, indicating alterations in immune cell function. Our findings provide new knowledge necessary for the development of immunomodulatory therapy targeting the immune response after prolonged myocardial ischemia/reperfusion.

Indexed as

AnimalsChemokinesCyclosporineHumansHuman Umbilical Vein Endothelial CellsImmunity, CellularKiller Cells, NaturalLymph NodesMaleMice, Inbred C57BLMyocardial InfarctionMyocardial Reperfusion InjuryMyocardiumNeovascularization, PhysiologicNeutrophilsTime FactorsChemokinesCyclosporineangiogenesiscyclosporine Aimmune responseinflammatory cytokinesischemia reperfusionlate reperfusionmyocardial infarction

Identifiers

PMID30858476
PMCPMC6786364
OpenAlexW2920831650

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.