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Updated: Feb 6, 2026

A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors
Published on: March 15, 2016
The Role of Vascular Endothelial Growth Factor in Systemic Sclerosis
Victoria A Flower1,2, Shaney L Barratt3,4, Stephen Ward2
1Royal National Hospital for Rheumatic Disease, Royal United Hospitals NHS Foundation Trusts, Bath, BA1 1RL United Kingdom.
Abstract:
The pathological hallmarks of Systemic Sclerosis (SSc) constitute an inter-related triad of autoimmunity, vasculopathy and tissue remodeling. Many signaling mediators have been implicated in SSc pathology; most focusing on individual components of this pathogenic triad and current treatment paradigms tend to approach management of such as distinct entities. The present review shall examine the role of Vascular Endothelial Growth Factor (VEGF) in SSc pathogenesis. We shall outline potential mechanisms whereby differential Vascular Endothelial Growth Factor-A (VEGF-A) isoform expression (through conventional and alternative VEGF-A splicing,) may influence the relevant burden of vasculopathy and fibrosis offering novel insight into clinical heterogeneity and disease progression in SSc. Emerging therapeutic approaches targeting VEGF signaling pathways might play an important role in the management of SSc, and differential VEGF-A splice isoform expression may provide a tool for personalized medicine approaches to disease management.
Insights
Systemic Sclerosis (SSc) involves autoimmunity, vasculopathy, and fibrosis. This review explores how Vascular Endothelial Growth Factor-A (VEGF-A) isoforms impact SSc, potentially guiding personalized treatments.
Area of Science:
- Immunology
- Vascular Biology
- Fibrosis Research
Background:
- Systemic Sclerosis (SSc) is characterized by autoimmunity, vasculopathy, and tissue remodeling.
- Current SSc treatments often address these aspects separately.
- Vascular Endothelial Growth Factor (VEGF) signaling is implicated in SSc pathogenesis.
Purpose of the Study:
- To review the role of Vascular Endothelial Growth Factor (VEGF) in Systemic Sclerosis (SSc).
- To explore how differential expression of Vascular Endothelial Growth Factor-A (VEGF-A) isoforms influences SSc vasculopathy and fibrosis.
- To provide insight into SSc clinical heterogeneity and disease progression.
Main Methods:
- Literature review focusing on VEGF and its isoforms in SSc.
- Analysis of potential mechanisms linking VEGF-A splicing to SSc pathology.
- Examination of emerging VEGF-targeted therapies for SSc.
Main Results:
- Differential expression of VEGF-A splice isoforms may contribute to SSc vasculopathy and fibrosis.
- VEGF-A isoform variations could explain clinical heterogeneity and disease progression in SSc.
- Targeting VEGF signaling presents a potential therapeutic avenue for SSc.
Conclusions:
- VEGF-A isoform expression is a key factor in SSc pathogenesis, affecting vasculopathy and fibrosis.
- Understanding VEGF-A splicing offers insights into SSc heterogeneity and progression.
- Targeting VEGF pathways, considering specific isoforms, may enable personalized SSc medicine.
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