Evidence map›Paper›PMID 32377427›Full record

ReviewCardiology research and practice2020

Macrophage Activities in Myocardial Infarction and Heart Failure.

Sophia Esi Duncan, Shan Gao, Michael Sarhene, Joel Wake Coffie, Deng Linhua, Xingru Bao, Zhang Jing, Sheng Li, Rui Guo, Jing Su and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Cardiology research and practice, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

48 citing papers in PubMed, 65 citations in OpenAlex.

  1. Simultaneous 3-D Adiabatic TNMR in biomedicine · 2026
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  5. Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026
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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

11 authors at 2 institutions in 1 country.

Sophia Esi DuncanFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Shan GaoFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Michael SarheneFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.ORCID https://orcid.org/0000-0001-8055-2435
Joel Wake CoffieState Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.ORCID https://orcid.org/0000-0002-8601-5195
Deng LinhuaFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Xingru BaoFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Zhang JingFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Sheng LiFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Rui GuoFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Jing SuFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.ORCID https://orcid.org/0000-0001-7962-0648
Guanwei FanFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.ORCID https://orcid.org/0000-0002-6066-2837
Tianjin University of Traditional Chinese Medicine · CNFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart diseases remain the major cause of death worldwide. Advances in pharmacological and biomedical management have resulted in an increasing proportion of patients surviving acute heart failure (HF). However, many survivors of HF in the early stages end up increasing the disease to chronic HF (CHF). HF is an established frequent complication of myocardial infarction (MI), and numerous influences including persistent myocardial ischemia, shocked myocardium, ventricular remodeling, infarct size, and mechanical impairments, as well as hibernating myocardium trigger the development of left ventricular systolic dysfunction following MI. Macrophage population is active in inflammatory process, yet the clear understanding of the causative roles for these macrophage cells in HF development and progression is actually incomplete. Long ago, it was thought that macrophages are of importance in the heart after MI. Also, though inflammation is as a result of adverse HF in patients, but despite the fact that broad immunosuppression therapeutic target has been used in various clinical trials, no positive results have showed up, but rather, the focus on proinflammatory cytokines has proved more benefits in patients with HF. Therefore, in this review, we discuss the recent findings and new development about macrophage activations in HF, its role in the healthy heart, and some therapeutic targets for myocardial repair. We have a strong believe that there is a need to give maximum attention to cardiac resident macrophages due to the fact that they perform various tasks in wound healing, self-renewal of the heart, and tissue remodeling. Currently, it has been discovered that the study of macrophages goes far beyond its phagocytotic roles. If researchers in future confirm that macrophages play a vital role in the heart, they can be therapeutically targeted for cardiac healing.

Identifiers

PMID32377427
PMCPMC7193281
OpenAlexW3017936190

What OpenQuestion holds

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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.