Thus, either the downregulation of TRPC-1 or the preferential binding of the upregulated anti-angiogenic VEGF165b isoform to VEGFR-2 may prevent the formation of the VEGF165/VEGFR-2/TRPC-1/sKl molecular complex on the plasma membrane of SSc-MVECs, contributing to cell dysfunction and impairment of angiogenesis. This evidence concerns the gene KDR and systemic sclerosis.