The crowded crossroad to angiogenesis in systemic sclerosis: where is the key to the problem?

Author: Mirko Manetti, Serena Guiducci and Marco Matucci-Cerinic
Date Published: January-2016
Source: Arthritis Research & Therapy

Dysregulated expression of several proangiogenic and antiangiogenic factors has been implicated in the dysfunction of angiogenesis in systemic sclerosis (SSc). Into this complex scenario comes the study recently published in Arthritis Research & Therapy by Hirigoyen et al. [1], who report new data implicating an inhibitory splice variant of vascular endothelial growth factor (VEGF)-A, namely VEGF165b, in the inhibition of angiogenesis by platelets in SSc. These findings are part of an intriguing chain of data as several studies have shown that VEGF-A, one of the most potent promoters of angiogenesis, is markedly increased in SSc skin and circulation despite clear evidence of an insufficient angiogenic response [2, 3].