Evidence map›Paper›PMID 27959619›Full record

ReviewAnnual review of physiology2017

Macrophages and the Recovery from Acute and Chronic Inflammation.

Kajal Hamidzadeh, Stephen M Christensen, Elizabeth Dalby, Prabha Chandrasekaran, David M Mosser

Open access · bronzeAbstract readReview
In one paragraph

Review in Annual review of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 224 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
224citing papers in PubMed, 1 pooled it
8.6field-weighted citation impact, top 2% 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

224 citing papers in PubMed, 1 synthesis or guideline pooled it, 422 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. A novelLife science alliance · 2026
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164 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

5 authors at 1 institution in 1 country.

Kajal HamidzadehDepartment of Cell Biology and Molecular Genetics, Maryland Pathogen Research Institute, University of Maryland, College Park, Maryland 20742; email: dmosser@umd.edu.
Stephen M ChristensenDepartment of Cell Biology and Molecular Genetics, Maryland Pathogen Research Institute, University of Maryland, College Park, Maryland 20742; email: dmosser@umd.edu.
Elizabeth DalbyDepartment of Cell Biology and Molecular Genetics, Maryland Pathogen Research Institute, University of Maryland, College Park, Maryland 20742; email: dmosser@umd.edu.
Prabha ChandrasekaranDepartment of Cell Biology and Molecular Genetics, Maryland Pathogen Research Institute, University of Maryland, College Park, Maryland 20742; email: dmosser@umd.edu.
David M MosserDepartment of Cell Biology and Molecular Genetics, Maryland Pathogen Research Institute, University of Maryland, College Park, Maryland 20742; email: dmosser@umd.edu.
University of Maryland, College Park · US

Funding

Training in Host-pathogens interactionsT32AI089621 · NIAID · UNIV OF MARYLAND, COLLEGE PARK · PI LEE, VINCENT T, MCIVER, KEVIN S. · 2010 to 2025
$2.1M
Regulatory macrophages and the host inflammatory responseR01GM102589 · NIGMS · UNIV OF MARYLAND, COLLEGE PARK · PI MOSSER, DAVID M · 2013 to 2016
$1.2M
NIAID NIH HHS T32 AI089621NIGMS NIH HHS R01 GM102589
6 · The paper itself

Abstract

In recent years, researchers have devoted much attention to the diverse roles of macrophages and their contributions to tissue development, wound healing, and angiogenesis. What should not be lost in the discussions regarding the diverse biology of these cells is that when perturbed, macrophages are the primary contributors to potentially pathological inflammatory processes. Macrophages stand poised to rapidly produce large amounts of inflammatory cytokines in response to danger signals. The production of these cytokines can initiate a cascade of inflammatory mediator release that can lead to wholesale tissue destruction. The destructive inflammatory capability of macrophages is amplified by exposure to exogenous interferon-γ, which prolongs and heightens inflammatory responses. In simple terms, macrophages can thus be viewed as incendiary devices with hair triggers waiting to detonate. We have begun to ask questions about how these cells can be regulated to mitigate the collateral destruction associated with macrophage activation.

Indexed as

AnimalsCytokinesHumansInflammationInterferon-gammaMacrophagesCytokinesInterferon-gammaadenosinecytokinesNF-κBprostaglandinTLRtranscription

Identifiers

PMID27959619
PMCPMC5912892
OpenAlexW2467662596

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.