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Updated: Nov 11, 2025

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
Published on: August 3, 2018
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.
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.
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.
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