Evidence map›Paper›PMID 38088942›Full record

ReviewJournal of inflammation research2023

Macrophage Heterogeneity and Its Impact on Myocardial Ischemia-Reperfusion Injury: An Integrative Review.

Shuwan Xu, Cong Xu, Jiahua Xu, Kun Zhang, Huanji Zhang

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of inflammation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
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  11. Sulfide regulation and catabolism in health and disease.Signal transduction and targeted therapy · 2025
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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

5 authors at 1 institution in 1 country.

Shuwan Xu *Cardiovascular Department, the Eighth Affiliated Hospital of Sun Yat-Sen University, Sun Yat-Sen University, Shenzhen, Guangdong, People's Republic of China.ORCID 0000-0001-7674-5154
Cong Xu *Cardiovascular Department, the Eighth Affiliated Hospital of Sun Yat-Sen University, Sun Yat-Sen University, Shenzhen, Guangdong, People's Republic of China.
Jiahua XuCardiovascular Department, the Eighth Affiliated Hospital of Sun Yat-Sen University, Sun Yat-Sen University, Shenzhen, Guangdong, People's Republic of China.ORCID 0009-0007-8206-5439
Kun ZhangDepartment of Cardiology, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University, Sun Yat-Sen University, Guangzhou, Guangdong, People's Republic of China.
Huanji ZhangCardiovascular Department, the Eighth Affiliated Hospital of Sun Yat-Sen University, Sun Yat-Sen University, Shenzhen, Guangdong, People's Republic of China.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The coronary reperfusion following acute myocardial infarction can paradoxically trigger myocardial ischemia-reperfusion (IR) injury. This complex phenomenon involves the intricate interplay of different subsets of macrophages. These macrophages are crucial players in the post-infarction inflammatory response and subsequent myocardial anti-inflammatory repair. However, their diverse functions can lead to both beneficial and detrimental effects. On one hand, these macrophages play a crucial role in orchestrating the inflammatory response, aiding in the clearance of cellular debris and initiating tissue repair mechanisms. On the other hand, their excessive infiltration and activation can contribute to the perpetuation of the inflammatory cascade, leading to additional myocardial injury and adverse cardiac remodeling. Multiple mechanisms contribute to the IR injury mediated by macrophages, including oxidative stress, apoptosis, and autophagy. These processes further exacerbate the damage to the already vulnerable myocardial tissue. To address this delicate balance, therapeutic strategies aiming to target and modulate macrophage polarization and function are being explored. By fine-tuning the immune inflammatory response, such interventions hold promise in mitigating post-infarction myocardial injury and fostering a more favorable environment for myocardial healing and recovery. Through advancements in this area of research, potential anti-inflammatory interventions may pave the way for improved clinical outcomes and better management of patients after acute myocardial infarction.

Indexed as

cardiac remodelinginflammatory cascadeischemia-reperfusion injurymacrophagesoxidative stress

Identifiers

PMID38088942
PMCPMC10712254
OpenAlexW4389441168

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.