Evidence map›Paper›PMID 20585340›Full record

ReviewNature reviews. Rheumatology2010

Cellular and molecular aspects of vascular dysfunction in systemic sclerosis.

Maria Trojanowska

Abstract readReview
In one paragraph

Review in Nature reviews. Rheumatology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 3 pooled it
3.0field-weighted citation impact, top 9% 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

109 citing papers in PubMed, 3 syntheses or guidelines pooled it, 218 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Direct in vivo reprogramming to relieve tissue ischemia via induced vasculogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Review
  13. Review
  14. Pericytes in tissue fibrosis.American journal of physiology. Cell physiology · 2025
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

49 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

1 author at 1 institution in 1 country.

Maria TrojanowskaBoston University School of Medicine, Arthritis Center, Boston, MA 02118, USA. trojanme@bu.edu
Boston University · US

Funding

The molecular mechanisms of fibrosisR01AR042334 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TROJANOWSKA, MARIA · 1994 to 2018
$5.2M
NIAMS NIH HHS R01 AR042334
6 · The paper itself

Abstract

Systemic sclerosis (SSc) is characterized by vascular alterations, activation of the immune system and tissue fibrosis. Vascular insufficiency manifests early in the disease, and although there is evidence of an active repair process, capillaries deteriorate and regress. Factors that contribute to the failure of vascular regeneration might include persistent injury, an imbalance between proangiogenic and antiangiogenic mediators, intrinsic abnormal properties of the cellular components of the vessels, and the presence of fibroblast-derived antiangiogenic factors. In addition, circulating dysfunctional endothelial progenitor cells might further exacerbate vessel deterioration. Abnormal expression of transcription factors, including Fra2 and Fli1, has been proposed to contribute to SSc vasculopathy. Fli1 regulates genes that are involved in vessel maturation and stabilization, suggesting that reduced levels of Fli1 in SSc vasculature could contribute to the development of unstable vessels that are prone to regression. Conversely, proliferating endothelial cells and pericytes, in the presence of an appropriate stimulus, might transdifferentiate into collagen-producing cells, and thus contribute to the initiation of fibrosis. Despite progress in treating the symptoms of vascular disease in SSc, the underlying mechanisms remain poorly understood. An improved knowledge of the molecular and cellular pathways that contribute to SSc vasculopathy could help in the design of effective therapies in the future.

Indexed as

AnimalsDisease Models, AnimalEndothelium, VascularFos-Related Antigen-2Gene ExpressionHumansMicrovesselsNeovascularization, PathologicProto-Oncogene Protein c-fli-1Scleroderma, SystemicVascular DiseasesFLI1 protein, humanFOSL2 protein, humanFos-Related Antigen-2Proto-Oncogene Protein c-fli-1

Identifiers

PMID20585340
PMCPMC3824624
OpenAlexW2007476135

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.