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Related Experiment Video

Updated: Jul 12, 2026

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice
08:09

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice

Published on: March 24, 2017

Therapeutic targets in systemic sclerosis.

Christopher P Denton1

  • 1Centre for Rheumatology, Royal Free and University College Medical School, Rowland Hill Street, London, NW3 2PF, UK. c.denton@medsch.ucl.ac.uk

Arthritis Research & Therapy
|September 15, 2007
PubMed
Summary

Systemic sclerosis (SSc) understanding has advanced, revealing pathogenic pathways and therapeutic targets. While profibrotic mediator therapies are pending, endothelin receptor antagonists show promise for vascular complications.

Related Experiment Videos

Last Updated: Jul 12, 2026

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice
08:09

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice

Published on: March 24, 2017

Area of Science:

  • Rheumatology
  • Immunology
  • Dermatology

Background:

  • Systemic sclerosis (SSc) aetiology is complex and not fully understood.
  • Clinical heterogeneity exists between diffuse and limited cutaneous SSc subsets.
  • Key pathogenic pathways and mediators are being identified as potential therapeutic targets.

Purpose of the Study:

  • To review advances in understanding SSc pathogenesis.
  • To identify potential therapeutic targets for SSc.
  • To evaluate current and emerging treatment strategies for SSc.

Main Methods:

  • Review of recent scientific literature on SSc.
  • Analysis of pathogenic pathways and molecular mediators.
  • Evaluation of clinical trial data for SSc therapies.

Main Results:

  • Advances in understanding SSc pathogenesis have identified key pathways.
  • Therapies targeting profibrotic mediators (e.g., CTGF, TGF-β) are under investigation.
  • Bosentan, an endothelin receptor antagonist, effectively manages SSc-related pulmonary arterial hypertension and digital ulcers.

Conclusions:

  • Despite challenges, progress in understanding SSc pathogenesis offers potential therapeutic avenues.
  • Targeting common mediators may benefit both diffuse and limited SSc subtypes.
  • Further research is needed to determine if newly identified mediators can be effectively manipulated for patient management.