Evidence map›Paper›PMID 25792449›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2015

Monocytes in myocardial infarction.

Partha Dutta, Matthias Nahrendorf

Open access · bronzeAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
135citing papers in PubMed, 4 pooled it
14.0field-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

135 citing papers in PubMed, 4 syntheses or guidelines pooled it, 209 citations in OpenAlex.

  1. Pooled it
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  16. Can Nuclear Imaging Detect Trained Immunity in Cardiovascular Disease?Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  17. Article
  18. Article
  19. Pannexins in the vasculature.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  20. Article

75 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

2 authors at 1 institution in 1 country.

Partha DuttaFrom the Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston. Dutta.Partha@mgh.harvard.edu.
Matthias NahrendorfFrom the Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston.
Center for Systems Biology · US

Funding

Dynamic interactions between ischemic stroke, immunity and the bone marrowR01NS084863 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI MOSKOWITZ, MICHAEL A., NAHRENDORF, MATTHIAS · 2014 to 2018
$3.2M
PET/MRI of cardiac repairR01HL096576 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NAHRENDORF, MATTHIAS · 2009 to 2017
$2.8M
Cell-Cell Interaction in Heart FailureR01HL117829 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NAHRENDORF, MATTHIAS · 2014 to 2017
$1.7M
Pathogen specific imaging of endocarditisR01HL114477 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI NAHRENDORF, MATTHIAS, PANIZZI, PETER ROLF · 2013 to 2016
$1.7M
Effect of diabetes on myelopoiesis and atherosclerosisK99HL121076 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI DUTTA, PARTHA · 2014 to 2015
$273k
NCI NIH HHS N02 PC015105NHLBI NIH HHS K99 HL121076NHLBI NIH HHS K99HL121076NHLBI NIH HHS R01 HL096576NHLBI NIH HHS R01HL096576NHLBI NIH HHS R01 HL114477NHLBI NIH HHS R01HL114477NHLBI NIH HHS R01 HL117829NHLBI NIH HHS R01HL117829NINDS NIH HHS R01 NS084863NINDS NIH HHS R01NS084863
6 · The paper itself

Abstract

Myocardial infarction (MI) is the leading cause of death in developed countries. Though timely revascularization of the ischemic myocardium and current standard therapy reduce acute mortality after MI, long-term morbidity and mortality remain high. During the first 1 to 2 weeks after MI, tissues in the infarcted myocardium undergo rapid turnover, including digestion of extracellular matrix and fibrosis. Post-MI repair is crucial to survival. Monocytes recruited to the infarcted myocardium remove debris and facilitate the repair process. However, exaggerated inflammation may also impede healing, as demonstrated by the association between elevated white blood cell count and in-hospital mortality after MI. Monocytes produced in the bone marrow and spleen enter the blood after MI and are recruited to the injured myocardium in 2 phases. The first phase is dominated by Ly-6c(high) monocytes and the second phase by Ly-6c(low) monocytes. Yet the number of Ly6C(low) monocytes recruited to the infarct is much lower, and Ly6C(high) monocytes can differentiate to Ly6C(low) macrophages in later healing stages. Understanding the signals regulating monocytosis after MI will help design new therapies to facilitate cardiac healing and limit heart failure.

Indexed as

Cell MovementExtracellular MatrixFemaleHematopoiesisHumansMacrophagesMaleMonocytesMyocardial InfarctionWound Healinghematopoiesismacrophagesmonocytesmyocardial infarction

Identifiers

PMID25792449
PMCPMC4409536
OpenAlexW2081004896

What OpenQuestion holds

Textmetadata
LicenceTDM
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.