ArticleFibrogenesis & tissue repair2012
Loss of PPARγ expression by fibroblasts enhances dermal wound closure.
Article in Fibrogenesis & tissue repair, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
The trial behind it
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Who cites it
12 citing papers in PubMed, 47 citations in OpenAlex.
- 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 · 2025Article
- CILP1 interacting with YBX1 promotes hypertrophic scar formation by suppressing PPARs transcription.Cell death & disease · 2025Article
- Hypoxia Preconditioned Serum Hydrogel (HPS-H) Accelerates Dermal Regeneration in a Porcine Wound Model.Gels (Basel, Switzerland) · 2024Article
- TEM1/endosialin/CD248 promotes pathologic scarring and TGF-β activity through its receptor stability in dermal fibroblasts.Journal of biomedical science · 2024Article
- Biomarkers in the Pathogenesis, Diagnosis, and Treatment of Systemic Sclerosis.Journal of inflammation research · 2023Review
- Roles of CCN2 as a mechano-sensing regulator of chondrocyte differentiation.The Japanese dental science review · 2020Review
- Mechanisms of carbon nanotube-induced pulmonary fibrosis: a physicochemical characteristic perspective.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2018Review
- Selective deletion of PPARβ/δ in fibroblasts causes dermal fibrosis by attenuated LRG1 expression.Cell discovery · 2018Article
- The Role of PPAR Gamma in Systemic Sclerosis.PPAR research · 2015Review
- The role of nuclear hormone receptors in cutaneous wound repair.Cell biochemistry and function · 2015Review
- Thrombospondin-1 mediates oncogenic Ras-induced senescence in premalignant lung tumors.The Journal of clinical investigation · 2013Article
- The Contribution of Peroxisome Proliferator-Activated Receptor Gamma to Cutaneous Wound Healing.Advances in wound care · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPeroxisome proliferator-activated receptor (PPAR)γ may be a key regulator of connective tissue deposition and remodeling in vivo. PPARγ expression is reduced in dermal fibroblasts isolated from fibrotic areas of scleroderma patients; PPARγ agonists suppress the persistent fibrotic phenotype of this cell type. Previously, we showed that loss of PPARγ expression in fibroblasts resulted in enhanced bleomycin-induced skin fibrosis. However, whether loss of PPARγ expression in skin fibroblasts affects cutaneous tissue repair or homeostasis is unknown.
resultsMice deleted for PPARγ in skin fibroblasts show an enhanced rate of dermal wound closure, concomitant with elevated phosphorylation of Smad3, Akt and ERK, and increased expression of proliferating cell nuclear antigen (PCNA), collagen, α-smooth muscle actin (α-SMA) and CCN2. Conversely, dermal homeostasis was not appreciably affected by loss of PPARγ expression.
conclusionPPARγ expression by fibroblasts suppresses cutaneous tissue repair. In the future, direct PPARγ antagonists and agonists might be of clinical benefit in controlling chronic wounds or scarring, respectively.
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Registered trials
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.