Evidence map›Paper›PMID 25590807›Full record

ArticleCell death & disease2015

Macrophage peroxisome proliferator-activated receptor γ deficiency delays skin wound healing through impairing apoptotic cell clearance in mice.

H Chen, R Shi, B Luo, X Yang, L Qiu, J Xiong, M Jiang, Y Liu, Z Zhang, Y Wu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
5.4field-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

66 citing papers in PubMed, 106 citations in OpenAlex.

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  12. Regulation of macrophage transcriptional dynamics during acute and chronic wound repair.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  13. Article
  14. Article
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6 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

10 authors at 1 institution in 1 country.

H ChenDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, Chongqing, China.
R ShiDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, Chongqing, China.
B LuoDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, Chongqing, China.
X YangDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, Chongqing, China.
L QiuDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, Chongqing, China.
J XiongDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, Chongqing, China.
M JiangDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, Chongqing, China.
Y LiuDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, Chongqing, China.
Z ZhangDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, Chongqing, China.
Y WuDepartment of Basic Medicine, Institute of Immunology, Third Military Medical University of PLA, Chongqing, China.
Army Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skin wound macrophages are key regulators of skin repair and their dysfunction causes chronic, non-healing skin wounds. Peroxisome proliferator-activated receptor gamma (PPARγ) regulates pleiotropic functions of macrophages, but its contribution in skin wound healing is poorly defined. We observed that macrophage PPARγ expression was upregulated during skin wound healing. Furthermore, macrophage PPARγ deficiency (PPARγ-knock out (KO)) mice exhibited impaired skin wound healing with reduced collagen deposition, angiogenesis and granulation formation. The tumor necrosis factor alpha (TNF-α) expression in wounds of PPARγ-KO mice was significantly increased and local restoration of TNF-α reversed the healing deficit in PPARγ-KO mice. Wound macrophages produced higher levels of TNF-α in PPARγ-KO mice compared with control. In vitro, the higher production of TNF-α by PPARγ-KO macrophages was associated with impaired apoptotic cell clearance. Correspondingly, increased apoptotic cell accumulation was found in skin wound of PPARγ-KO mice. Mechanically, peritoneal and skin wound macrophages expressed lower levels of various phagocytosis-related molecules. In addition, PPARγ agonist accelerated wound healing and reduced local TNF-α expression and wound apoptotic cells accumulation in wild type but not PPARγ-KO mice. Therefore, PPARγ has a pivotal role in controlling wound macrophage clearance of apoptotic cells to ensure efficient skin wound healing, suggesting a potential new therapeutic target for skin wound healing.

Indexed as

ApoptosisWound HealingAnimalsCell CountGene Expression RegulationInflammationMacrophagesMaleMice, Inbred C57BLMice, KnockoutNeutrophilsPhagocytosisPPAR gammaRNA, MessengerSkinTumor Necrosis Factor-alphaPPAR gammaRNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID25590807
PMCPMC4669743
OpenAlexW2009660839

What OpenQuestion holds

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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.