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.
Original language | English |
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Pages (from-to) | 99-109 |
Number of pages | 11 |
Journal | Current Rheumatology Reviews |
Volume | 15 |
Issue number | 2 |
Early online date | 9 Aug 2018 |
DOIs | |
Publication status | Published - 2019 |
Bibliographical note
Copyright© Bentham Science Publishers; For any queries, please email at [email protected].Keywords
- Anti-angiogenic
- Fibrosis
- Pathogenesis
- Pro-fibrotic
- Systemic sclerosis (scleroderma)
- VEGF-A
- VEGF-AB
- Vascular endothelial growth factor
- Vasculopathy
- Humans
- Scleroderma, Systemic/metabolism
- Vascular Endothelial Growth Factor A/metabolism
- Protein Isoforms
ASJC Scopus subject areas
- Rheumatology