Evidence map›Paper›PMID 31109146›Full record

ReviewInternational journal of molecular sciences2019

Role of Macrophages in Cardioprotection.

Jonathan Yap, Hector A Cabrera-Fuentes, Jason Irei, Derek J Hausenloy, William A Boisvert

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
6.1field-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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

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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 2 institutions in 6 countries.

Jonathan YapCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI 96813, USA. jktyap@hawaii.edu.
Hector A Cabrera-FuentesTecnologico de Monterrey, Centro de Biotecnologia-FEMSA, Monterrey, NL 264610, Mexico. hacafu@tec.mx.
Jason IreiCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI 96813, USA. jasonsi@hawaii.edu.
Derek J HausenloyNational Heart Research Institute Singapore, National Heart Centre, Singapore 169609, Singapore. d.hausenloy@ucl.ac.uk.
William A BoisvertCenter for Cardiovascular Research, John A. Burns School of Medicine, University of Hawaii, Honolulu, HI 96813, USA. wab@hawaii.edu.ORCID 0000-0003-2574-9176
University of Hawaiʻi at Mānoa · USNational University of Singapore · SG

Funding

The Role of gp120 on Cardiovascular Disease in People Living with HIVU54MD007601 · NIMHD · UNIVERSITY OF HAWAII AT MANOA · PI Benjamin C. Fogelgren · 2017 to 2026
$59.5M
NIMHD NIH HHS U54 MD007601
6 · The paper itself

Abstract

Cardiovascular diseases are the leading cause of mortality worldwide. It is widely known that non-resolving inflammation results in atherosclerotic conditions, which are responsible for a host of downstream pathologies including thrombosis, myocardial infarction (MI), and neurovascular events. Macrophages, as part of the innate immune response, are among the most important cell types in every stage of atherosclerosis. In this review we discuss the principles governing macrophage function in the healthy and infarcted heart. More specifically, how cardiac macrophages participate in myocardial infarction as well as cardiac repair and remodeling. The intricate balance between phenotypically heterogeneous populations of macrophages in the heart have profound and highly orchestrated effects during different phases of myocardial infarction. In the early "inflammatory" stage of MI, resident cardiac macrophages are replaced by classically activated macrophages derived from the bone marrow and spleen. And while the macrophage population shifts towards an alternatively activated phenotype, the inflammatory response subsides giving way to the "reparative/proliferative" phase. Lastly, we describe the therapeutic potential of cardiac macrophages in the context of cell-mediated cardio-protection. Promising results demonstrate innovative concepts; one employing a subset of yolk sac-derived, cardiac macrophages that have complete restorative capacity in the injured myocardium of neonatal mice, and in another example, post-conditioning of cardiac macrophages with cardiosphere-derived cells significantly improved patient's post-MI diagnoses.

Indexed as

Immunity, InnateAnimalsCardiovascular DiseasesHeartHumansMacrophagesMyocardial InfarctionMyocardiumProtective FactorsVentricular Remodelingcardiac repaircardioprotectioninnate immune responsemacrophagesmyocardial infarctionremodeling

Identifiers

PMID31109146
PMCPMC6566352
OpenAlexW2945020041

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.