Vascular Remodelling and Mesenchymal Transition in Systemic Sclerosis

Area of Science:

• Cardiovascular Biology
• Immunology
• Dermatology

Background:

• Systemic Sclerosis (SSc) is characterized by fibrosis, autoimmunity, and vascular inflammation.
• Early SSc features include endothelial cell injury, intimal hyperplasia, and vascular lumen obliteration.
• Reduced blood flow, deficient angiogenesis, and fibrosis contribute to chronic hypoxia and vascular remodeling.

Purpose of the Study:

• To review molecular pathways involved in SSc vasculopathy.
• To explore the role of sustained vascular inflammation on vascular cell plasticity.
• To focus on endothelial-mesenchymal transition (EndMT) as a potential therapeutic target.

Main Methods:

• Literature review of molecular pathways in SSc pathogenesis.
• Analysis of the role of signaling pathways (TGF-β, Wnt, Notch) in EndMT.
• Examination of EndMT reversibility in vascular remodeling.

Main Results:

• Endothelial-mesenchymal transition is implicated in SSc vasculopathy.
• Transforming growth factor-beta, Wnt, and Notch signaling pathways are key regulators of EndMT.
• Evidence suggests that EndMT may be a reversible process.

Conclusions:

• Endothelial-mesenchymal transition is a critical process in SSc vasculopathy.
• Targeting signaling pathways regulating EndMT could offer novel therapeutic strategies for SSc.
• The potential reversibility of EndMT presents a promising avenue for future SSc treatments.