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Endothelial-to-mesenchymal transition in systemic sclerosis.

P Di Benedetto1, P Ruscitti2, O Berardicurti2

  • 1Clinical Pathology Unit, Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy.

Clinical and Experimental Immunology
|March 27, 2021
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Summary

Systemic sclerosis involves microvascular damage where endothelial cells (ECs) transform into myofibroblasts via endothelial-to-mesenchymal transition (EndMT), driving fibrosis. Understanding EndMT mechanisms offers new therapeutic targets for this autoimmune disease.

Keywords:
endothelial cellsendothelial-to-mesenchymal transitionsystemic sclerosis

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Area of Science:

  • Immunology
  • Pathology
  • Vascular Biology

Background:

  • Systemic sclerosis (SSc) is an autoimmune disease marked by vascular issues and fibrosis.
  • Microvascular changes are an early SSc hallmark.
  • Endothelial cells (ECs) are implicated in fibrosis development.

Purpose of the Study:

  • To review the molecular mechanisms of endothelial-to-mesenchymal transition (EndMT).
  • To summarize EndMT's role in SSc-related fibrosis.
  • To explore therapeutic strategies targeting EndMT inhibition.

Main Methods:

  • Literature review focusing on molecular pathways.
  • Analysis of existing evidence on EndMT in SSc pathogenesis.
  • Exploration of potential therapeutic interventions.

Main Results:

  • EndMT is a key process where injured ECs become myofibroblasts.
  • This transition contributes significantly to collagen deposition and fibrosis in SSc.
  • Molecular mechanisms driving EndMT are increasingly understood.

Conclusions:

  • EndMT is a critical pathogenetic event in systemic sclerosis.
  • Targeting EndMT presents a promising therapeutic avenue for SSc.
  • Further research into EndMT inhibition could lead to novel treatments.