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Pathophysiology of systemic sclerosis.

Benjamin Thoreau1, Benjamin Chaigne1, Arthur Renaud2

  • 1Institut Cochin, Inserm U1016, CNRS UMR 8104,Université de Paris, Paris, France; Service de Médecine Interne, Centre de Référence Maladies Systémiques Autoimmunes Rares d'Ile de France, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France.

Presse Medicale (Paris, France : 1983)
|October 31, 2021
PubMed
Summary
This summary is machine-generated.

Systemic sclerosis (SSc) is a rare autoimmune disease involving fibrosis and vascular issues. Research explores genetic, environmental, and epigenetic factors, plus animal models, to understand SSc pathogenesis and develop new therapies.

Keywords:
AutoimmunityEndotheliumFibroblastsPathophysiologySystemic sclerosis

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Area of Science:

  • Immunology
  • Rheumatology
  • Pathology

Background:

  • Systemic sclerosis (SSc) is a rare autoimmune connective tissue disease.
  • It is characterized by vascular remodeling, fibroblast activation, excessive extracellular matrix production, and autoimmunity.
  • Environmental (silica, solvents), genetic (IRF5, STAT4), and epigenetic factors (histone modifications, DNA hypomethylation, non-coding RNAs) are implicated in SSc pathogenesis.

Purpose of the Study:

  • To understand the complex mechanisms contributing to vasculopathy and fibrosis in Systemic Sclerosis.
  • To review the role of various cellular and molecular actors in SSc pathophysiology.
  • To identify potential therapeutic targets for SSc.

Main Methods:

  • Review of existing literature on Systemic Sclerosis.
  • Analysis of data from human SSc patients.
  • Examination of various animal models of SSc (genetic and induced).

Main Results:

  • SSc involves dysregulation of innate and adaptive immune cells and fibroblasts.
  • Pro-inflammatory and pro-fibrosing pathways (Wnt, TGF-β) and oxidative stress play significant roles.
  • Fibroblast overactivity, genetic dysregulation, apoptosis defects, and extracellular matrix overproduction lead to vasculopathy and fibrosis.

Conclusions:

  • Advances in understanding SSc mechanisms are paving the way for new therapeutic strategies.
  • Targeting cellular and molecular pathways involved in SSc pathogenesis offers potential for novel treatments.
  • Development of biologics and small molecules represents promising therapeutic avenues for SSc.