Evidence map›Paper›PMID 37170235›Full record

ReviewCell communication and signaling : CCS2023

Crosstalk between macrophages and cardiac cells after myocardial infarction.

Yuhong Jian, Xiao Zhou, Wenju Shan, Cheng Chen, Wei Ge, Jun Cui, Wei Yi, Yang Sun

Open access · goldAbstract readVideo-Audio MediaReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 1 pooled it
18.7field-weighted citation impact, top 1% 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

63 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  7. Article
  8. Regenerative therapy · 2026
    Article
  9. Article
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  12. Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026
    Review
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3 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 1 country.

Yuhong Jian *Department of General Medicine, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Xiao Zhou *Department of Anesthesiology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wenju ShanDepartment of General Medicine, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Cheng ChenDepartment of General Medicine, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Wei GeDepartment of General Medicine, Xijing Hospital, The Fourth Military Medical University, Xi'an, China.
Jun CuiDepartment of Cardiovascular Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China. cuijun1021@yeah.net.
Wei YiDepartment of Cardiovascular Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, China. yiwei@fmmu.edu.
Yang SunDepartment of General Medicine, Xijing Hospital, The Fourth Military Medical University, Xi'an, China. drsunyang@fmmu.edu.cn.
Air Force Medical University · CNXijing Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular diseases, such as myocardial infarction (MI), are a leading cause of death worldwide. Acute MI (AMI) inflicts massive injury to the coronary microcirculation, causing large-scale cardiomyocyte death due to ischemia and hypoxia. Inflammatory cells such as monocytes and macrophages migrate to the damaged area to clear away dead cells post-MI. Macrophages are pleiotropic cells of the innate immune system, which play an essential role in the initial inflammatory response that occurs following MI, inducing subsequent damage and facilitating recovery. Besides their recognized role within the immune response, macrophages participate in crosstalk with other cells (including cardiomyocytes, fibroblasts, immune cells, and vascular endothelial cells) to coordinate post-MI processes within cardiac tissue. Macrophage-secreted exosomes have recently attracted increasing attention, which has led to a more elaborate understanding of macrophage function. Currently, the functional roles of macrophages in the microenvironment of the infarcted heart, particularly with regard to their interaction with surrounding cells, remain unclear. Understanding the specific mechanisms that mediate this crosstalk is essential in treating MI. In this review, we discuss the origin of macrophages, changes in their distribution post-MI, phenotypic and functional plasticity, as well as the specific signaling pathways involved, with a focus on the crosstalk with other cells in the heart. Thus, we provide a new perspective on the treatment of MI. Further in-depth research is required to elucidate the mechanisms underlying crosstalk between macrophages and other cells within cardiac tissue for the identification of potential therapeutic targets. Video Abstract.

Indexed as

Endothelial CellsMyocardial InfarctionAnimalsHumansMacrophagesMiceMice, Inbred C57BLMonocytesMyocardiumMyocytes, CardiacCrosstalkMacrophagesMyocardial infarctionSignaling pathway

Identifiers

PMID37170235
PMCPMC10173491
OpenAlexW4376226294

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.