Evidence map›Paper›PMID 25475596›Full record

ReviewCurrent rheumatology reports2015

Role of cellular senescence and NOX4-mediated oxidative stress in systemic sclerosis pathogenesis.

Sonsoles Piera-Velazquez, Sergio A Jimenez

Open access · greenAbstract readReview
In one paragraph

Review in Current rheumatology reports, 2015. 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
1.9field-weighted citation impact, top 16% 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, 51 citations in OpenAlex.

  1. Trial
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  15. Article
  16. Review
  17. Abrogation of transforming growth factor-β-induced tissue fibrosis in mice with a global genetic deletion of Nox4.Laboratory investigation; a journal of technical methods and pathology · 2019
    Article
  18. Oxidative stress in the pathogenesis of systemic scleroderma: An overview.Journal of cellular and molecular medicine · 2018
    Review
  19. Sirtuins and Accelerated Aging in Scleroderma.Current rheumatology reports · 2018
    Review
  20. Article
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

2 authors at 2 institutions in 1 country.

Sonsoles Piera-VelazquezScleroderma Center, Thomas Jefferson University, 233 South 10th Street, Suite 509 BLSB, Philadelphia, PA, 19107, USA.
Sergio A Jimenez
Jefferson Institute · USThomas Jefferson University · US

Funding

BIOCHEMICAL AND VASCULAR ALTERATIONS IN SCLERODERMAR01AR019616 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI JIMENEZ, SERGIO A · 1986 to 2010
$3.2M
NIAMS NIH HHS R01 AR019616NIAMS NIH HHS R01 AR019616-29
6 · The paper itself

Abstract

Systemic sclerosis (SSc) is a systemic autoimmune disease characterized by progressive fibrosis of skin and numerous internal organs and a severe fibroproliferative vasculopathy resulting frequently in severe disability and high mortality. Although the etiology of SSc is unknown and the detailed mechanisms responsible for the fibrotic process have not been fully elucidated, one important observation from a large US population study was the demonstration of a late onset of SSc with a peak incidence between 45 and 54 years of age in African-American females and between 65 and 74 years of age in white females. Although it is not appropriate to consider SSc as a disease of aging, the possibility that senescence changes in the cellular elements involved in its pathogenesis may play a role has not been thoroughly examined. The process of cellular senescence is extremely complex, and the mechanisms, molecular events, and signaling pathways involved have not been fully elucidated; however, there is strong evidence to support the concept that oxidative stress caused by the excessive generation of reactive oxygen species may be one important mechanism involved. On the other hand, numerous studies have implicated oxidative stress in SSc pathogenesis, thus, suggesting a plausible mechanism in which excessive oxidative stress induces cellular senescence and that the molecular events associated with this complex process play an important role in the fibrotic and fibroproliferative vasculopathy characteristic of SSc. Here, recent studies examining the role of cellular senescence and of oxidative stress in SSc pathogenesis will be reviewed.

Indexed as

Cellular SenescenceFibrosisHumansNADPH Oxidase 4NADPH OxidasesOxidative StressReactive Oxygen SpeciesScleroderma, SystemicNADPH Oxidase 4NADPH OxidasesNOX4 protein, humanReactive Oxygen Species

Identifiers

PMID25475596
PMCPMC6779060
OpenAlexW1995464047

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.