Evidence map›Paper›PMID 36627513›Full record

ReviewNature reviews. Cardiology2023

Macrophages in cardiac remodelling after myocardial infarction.

Jonathan Yap, Jason Irei, Javier Lozano-Gerona, Selena Vanapruks, Tianmai Bishop, William A Boisvert

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 184 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
184citing papers in PubMed, 1 pooled it
53.3field-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

184 citing papers in PubMed, 1 synthesis or guideline pooled it, 243 citations in OpenAlex.

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124 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

6 authors at 1 institution in 1 country.

Jonathan YapCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI, USA.
Jason IreiCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI, USA.ORCID 0000-0002-0538-9815
Javier Lozano-GeronaCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI, USA.ORCID 0000-0003-4867-2511
Selena VanapruksCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI, USA.
Tianmai BishopCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI, USA.
William A BoisvertCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI, USA. wab@hawaii.edu.ORCID 0000-0003-2574-9176
University of Hawaiʻi at Mānoa · US

Funding

Training in Cardiovascular Research at the University of HawaiiT32HL115505 · NHLBI · UNIVERSITY OF HAWAII AT MANOA · PI Michelle D Tallquist · 2012 to 2026
$3.8M
NHLBI NIH HHS T32 HL115505
6 · The paper itself

Abstract

Myocardial infarction (MI), as a result of thrombosis or vascular occlusion, is the most prevalent cause of morbidity and mortality among all cardiovascular diseases. The devastating consequences of MI are compounded by the complexities of cellular functions involved in the initiation and resolution of early-onset inflammation and the longer-term effects related to scar formation. The resultant tissue damage can occur as early as 1 h after MI and activates inflammatory signalling pathways to elicit an immune response. Macrophages are one of the most active cell types during all stages after MI, including the cardioprotective, inflammatory and tissue repair phases. In this Review, we describe the phenotypes of cardiac macrophage involved in MI and their cardioprotective functions. A specific subset of macrophages called resident cardiac macrophages (RCMs) are derived from yolk sac progenitor cells and are maintained as a self-renewing population, although their numbers decrease with age. We explore sophisticated sequencing techniques that demonstrate the cardioprotective properties of this cardiac macrophage phenotype. Furthermore, we discuss the interactions between cardiac macrophages and other important cell types involved in the pathology and resolution of inflammation after MI. We summarize new and promising therapeutic approaches that target macrophage-mediated inflammation and the cardioprotective properties of RCMs after MI. Finally, we discuss future directions for the study of RCMs in MI and cardiovascular health in general.

Indexed as

Myocardial InfarctionVentricular RemodelingHeartHumansInflammationMacrophagesMyocardium

Identifiers

PMID36627513
OpenAlexW4313988041

What OpenQuestion holds

Textmetadata
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.