Evidence map›Paper›PMID 22802908›Full record

ArticleThe open rheumatology journal2012

Regulation of Matrix Remodeling by Peroxisome Proliferator-Activated Receptor-γ: A Novel Link Between Metabolism and Fibrogenesis.

Jun Wei, Swati Bhattacharyya, Manu Jain, John Varga

Open access · hybridAbstract read
In one paragraph

Article in The open rheumatology journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Lobeglitazone attenuates fibrosis in corneal fibroblasts by interrupting TGF-beta-mediated Smad signaling.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022
    Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Interfacial Adipose Tissue in Systemic Sclerosis.Current rheumatology reports · 2017
    Review
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

4 authors at 2 institutions in 1 country.

Jun WeiDivision of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, USA.
Swati Bhattacharyya
Manu Jain
John Varga
Center for Rheumatology · USNorthwestern University · US

Funding

MULTIDISCIPLINARY CLINICAL AND TRANSLATIONAL SCIENCE (MCTS) PROGRAM (UL1)UL1RR025741 · NCRR · NORTHWESTERN UNIVERSITY AT CHICAGO · PI GREENLAND, PHILIP · 2008 to 2011
$24.7M
Multidisciplinary Clinical and Translational Science (MCTS) Program (UL1)UL1TR000150 · NCATS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LLOYD-JONES, DONALD M · 2012 to 2013
$10.1M
REGULATION OF COLLAGEN GENE EXPRESSION BY TGF-BETAR01AR042309 · NIAMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI VARGA, JOHN · 1994 to 2014
$4.4M
Aberrant TLR responses driving organ fibrosis in systemic sclerosisR56AR042309 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI VARGA, JOHN · 2018 to 2018
$477k
NCATS NIH HHS UL1 TR000150NCRR NIH HHS UL1 RR025741NIAMS NIH HHS R01 AR042309NIAMS NIH HHS R56 AR042309
6 · The paper itself

Abstract

The intractable process of fibrosis underlies the pathogenesis of systemic sclerosis (SSc) and other diseases, and in aggregate contributes to 45% of deaths worldwide. Because currently there is no effective anti-fibrotic therapy, a better understanding of the pathways and cellular differentiation programs underlying fibrosis are needed. Emerging evidence points to a fundamental role of the nuclear hormone receptor peroxisome proliferator activated receptor-γ (PPAR-γ) in modulating fibrogenesis. While PPAR-γ has long been known to be important in lipid metabolism and in glucose homeostasis, its role in regulating mesenchymal cell biology and its association with pathological fibrosis had not been appreciated until recently. This article highlights recent studies revealing a consistent association of fibrosis with aberrant PPAR-γ expression and activity in various forms of human fibrosis and in rodent models, and reviews studies linking genetic manipulation of the PPAR-γ pathway in rodents and fibrosis. We survey the broad range of anti-fibrotic activities associated with PPAR-γ and the underlying mechanisms. We also summarize the emerging data linking PPAR-γ dysfunction and pulmonary arterial hypertension (PAH), which together with fibrosis is responsible for the mortality in patients in SSc. Finally, we consider current and potential future strategies for targeting PPAR-γ activity or expression as a therapy for controlling fibrosis.

Indexed as

PPAR-γSPPARMsystemic sclerosisTGF-β.

Identifiers

PMID22802908
PMCPMC3396343
OpenAlexW2076354639

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.