Evidence map›Paper›PMID 32877204›Full record

ReviewAmerican journal of physiology. Cell physiology2020

Monocyte recruitment and fate specification after myocardial infarction.

Kyle I Mentkowski, Lindsey M Euscher, Akshar Patel, B Rita Alevriadou, Jennifer K Lang

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Cell physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.6field-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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

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  20. Cardiac macrophage metabolism in health and disease.Trends in endocrinology and metabolism: TEM · 2024
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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 3 institutions in 1 country.

Kyle I MentkowskiDepartment of Medicine, Division of Cardiology, Jacobs School of Medicine and Biomedical Sciences, Buffalo, New York.
Lindsey M EuscherDepartment of Medicine, Division of Cardiology, Jacobs School of Medicine and Biomedical Sciences, Buffalo, New York.
Akshar PatelDepartment of Biomedical Engineering, University at Buffalo, Buffalo, New York.
B Rita AlevriadouDepartment of Biomedical Engineering, University at Buffalo, Buffalo, New York.
Jennifer K LangDepartment of Medicine, Division of Cardiology, Jacobs School of Medicine and Biomedical Sciences, Buffalo, New York.ORCID 0000-0002-6221-8625
Jacobs Institute · USUniversity at Buffalo, State University of New York · USVA Western New York Healthcare System · US

Funding

Control of Endothelial Mechanotransduction by the Mitochondrial Ca2+ Uniporter: Implications for AtherosclerosisR01HL142673 · NHLBI · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI ALEVRIADOU, BARBARA RITA, MUNISWAMY, MADESH · 2018 to 2021
$2.0M
The Functional Role of Exosomes in Stem Cell-Mediated Cardiac RepairK08HL130594 · NHLBI · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI LANG, JENNIFER K · 2018 to 2018
$197k
BLRD VA IK2 BX004097HHS | National Institutes of Health (NIH) K08HL130594HHS | National Institutes of Health (NIH) R01HL142673NHLBI NIH HHS R01 HL142673
6 · The paper itself

Abstract

Monocytes are critical mediators of the inflammatory response following myocardial infarction (MI) and ischemia-reperfusion injury. They are involved in both initiation and resolution of inflammation and play an integral role in cardiac repair. The antagonistic nature of their function is dependent on their subset heterogeneity and biphasic response following injury. New advancements in single-cell transcriptomics and mass cytometry have allowed us to identify smaller, transcriptionally distinct clusters that may have functional relevance in disease and homeostasis. Additionally, recent insights into the spatiotemporal dynamics of monocytes following ischemic injury and their subsequent interactions with the endothelium and other immune cells reveal a complex interplay between monocytes and the cardiac milieu. In this review, we highlight recent findings on monocyte functional heterogeneity, present new mechanistic insight into monocyte recruitment and fate specification following MI, and discuss promising therapeutic avenues targeting monocytes for the treatment of ischemic heart disease.

Indexed as

AnimalsCell LineageChemokinesDisease Models, AnimalExosomesGene Expression RegulationHumansInflammationInterleukin 1 Receptor Antagonist ProteinInterleukinsIsoflavonesMiceMonocytesMyocardial InfarctionMyocardial Reperfusion InjuryReceptors, ChemokineChemokinesInterleukin 1 Receptor Antagonist ProteinInterleukinsIsoflavonespuerarinReceptors, ChemokineCCR2innate immune responsemonocytesmyocardial infarction

Identifiers

PMID32877204
PMCPMC7701269
OpenAlexW3081716042

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.