Evidence map›Paper›PMID 25875529›Full record

ArticleThe Journal of pathology2015

Macrophage PPARγ and impaired wound healing in type 2 diabetes.

Rita E Mirza, Milie M Fang, Margaret L Novak, Norifumi Urao, Audrey Sui, William J Ennis, Timothy J Koh

Abstract read
In one paragraph

Article in The Journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 1 pooled it
5.1field-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

95 citing papers in PubMed, 1 synthesis or guideline pooled it, 172 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. The Mechanistic Role of PPARPPAR research · 2026
    Review
  10. Review
  11. 12/15-lipoxygenase orchestrates murine wound healing via PPARγ-activating oxylipins acting holistically to dampen inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Review
  13. Poloxamer-based hydrogel with EGCG and rhEGF for diabetic foot ulcer treatment.Journal of materials science. Materials in medicine · 2025
    Article
  14. Effect of Fibroblast Signaling on Macrophage Polarization.The American journal of pathology · 2025
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review

35 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

7 authors at 2 institutions in 1 country.

Rita E MirzaDepartment of Kinesiology and Nutrition, University of Illinois, Chicago, IL, USA.
Milie M FangDepartment of Kinesiology and Nutrition, University of Illinois, Chicago, IL, USA.
Margaret L NovakDepartment of Kinesiology and Nutrition, University of Illinois, Chicago, IL, USA.
Norifumi UraoDepartment of Kinesiology and Nutrition, University of Illinois, Chicago, IL, USA.
Audrey SuiDepartment of Surgery, University of Illinois, Chicago, IL, USA.
William J EnnisDepartment of Surgery, University of Illinois, Chicago, IL, USA.
Timothy J KohDepartment of Kinesiology and Nutrition, University of Illinois, Chicago, IL, USA.
University of Illinois Chicago · USTissue Regeneration Systems (United States) · US

Funding

Macrophage Phenotype and Impaired Wound HealingR01GM092850 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI KOH, TIMOTHY J · 2011 to 2019
$3.5M
NIGMS NIH HHS R01 GM092850
6 · The paper itself

Abstract

Macrophages undergo a transition from pro-inflammatory to healing-associated phenotypes that is critical for efficient wound healing. However, the regulation of this transition during normal and impaired healing remains to be elucidated. In our studies, the switch in macrophage phenotypes during skin wound healing was associated with up-regulation of the peroxisome proliferator-activated receptor (PPAR)γ and its downstream targets, along with increased mitochondrial content. In the setting of diabetes, up-regulation of PPARγ activity was impaired by sustained expression of IL-1β in both mouse and human wounds. In addition, experiments with myeloid-specific PPARγ knockout mice indicated that loss of PPARγ in macrophages is sufficient to prolong wound inflammation and delay healing. Furthermore, PPARγ agonists promoted a healing-associated macrophage phenotype both in vitro and in vivo, even in the diabetic wound environment. Importantly, topical administration of PPARγ agonists improved healing in diabetic mice, suggesting an appealing strategy for down-regulating inflammation and improving the healing of chronic wounds.

Indexed as

Wound HealingAdministration, CutaneousAnimalsCells, CulturedDiabetes Mellitus, Type 1Disease Models, AnimalFemaleHumansInterleukin-1betaLeg UlcerMacrophagesMaleMice, Inbred C57BLMice, KnockoutPhenotypePPAR gamma15-deoxyprostaglandin J2IL1B protein, humanIL1B protein, mouseIL1R1 protein, mouseInterleukin-1betaPPAR gammaProstaglandin D2Receptors, Interleukin-1 Type IRosiglitazoneThiazolidinedionesdiabetesinflammationmacrophageresolution of inflammationwound healing

Identifiers

PMID25875529
PMCPMC4509817
OpenAlexW1596824448

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.