Evidence map›Paper›PMID 22566847›Full record

ArticleFrontiers in immunology2011

Modulation of macrophage efferocytosis in inflammation.

Darlynn Korns, S Courtney Frasch, Ruby Fernandez-Boyanapalli, Peter M Henson, Donna L Bratton

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
206citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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

206 citing papers in PubMed, 1 synthesis or guideline pooled it, 344 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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146 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 2 institutions in 1 country.

Darlynn KornsDivision of Cell Biology, Department of Pediatrics, National Jewish Health Denver, CO, USA.
S Courtney Frasch
Ruby Fernandez-Boyanapalli
Peter M Henson
Donna L Bratton
University of Colorado Denver · USNational Jewish Health · US

Funding

TRANSLOCATION AND TRANSCELLULAR BIOSYNTHESISP01HL034303 · NHLBI · NATIONAL JEWISH HEALTH · PI BRATTON, DONNA L · 1985 to 2015
$25.0M
Regulation of Pulmonary InflammationR01HL081151 · NHLBI · NATIONAL JEWISH HEALTH · PI HENSON, PETER M · 2005 to 2012
$3.5M
Uptake of apoptotic cellsR01GM061031 · NIGMS · NATIONAL JEWISH HEALTH · PI HENSON, PETER M · 2001 to 2009
$3.0M
Defective PS Exposure in Neutrophil Apoptosis in CGDR01AI058228 · NIAID · NATIONAL JEWISH HEALTH · PI BRATTON, DONNA L · 2004 to 2007
$1.0M
Macrophage PPARg signaling, efferocytosis, and exaggerated inflammation in CGDR56AI058228 · NIAID · NATIONAL JEWISH HEALTH · PI BRATTON, DONNA L · 2011 to 2011
$317k
NHLBI NIH HHS P01 HL034303NHLBI NIH HHS R01 HL081151NIAID NIH HHS R01 AI058228NIAID NIH HHS R56 AI058228NIGMS NIH HHS R01 GM061031
6 · The paper itself

Abstract

A critical function of macrophages within the inflammatory milieu is the removal of dying cells by a specialized phagocytic process called efferocytosis ("to carry to the grave"). Through specific receptor engagement and induction of downstream signaling, efferocytosing macrophages promote resolution of inflammation by (i) efficiently engulfing dying cells, thus avoiding cellular disruption and release of inflammatory contents, and (ii) producing anti-inflammatory mediators such as IL-10 and TGF-β that dampen pro-inflammatory responses. Evidence suggests that plasticity in macrophage programming, in response to changing environmental cues, modulates efferocytic capability. Essential to programming for enhanced efferocytosis is activation of the nuclear receptors PPARγ, PPARδ, LXR, and possibly RXRα. Additionally, a number of signals in the inflammatory milieu, including those from dying cells themselves, can influence efferocytic efficacy either by acting as immediate inhibitors/enhancers or by altering macrophage programming for longer-term effects. Importantly, sustained inflammatory programming of macrophages can lead to defective apoptotic cell clearance and is associated with development of autoimmunity and other chronic inflammatory disorders. This review summarizes the current knowledge of the multiple factors that modulate macrophage efferocytic ability and highlights emerging therapeutic targets with significant potential for limiting chronic inflammation.

Indexed as

alternative activationapoptotic cellclassical activationefferocytosisinflammationmacrophage

Identifiers

PMID22566847
PMCPMC3342042
OpenAlexW1986480779

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.