Furthermore, in combination with previous findings, this study suggested that regulation of NOS expression is susceptible to α-galactosidase A deficiency, and this may represent a general pathogenic mechanism of Fabry vasculopathy.
This fact may be important for the development of atherosclerotic lesions during chronic renal failure and is in accordance with recently published studies showing that under conditions with decreased constitutive NOS activity, iNOS might substitute the synthesis of NO. iNOS expression in vascular smooth muscle cells and macrophages is supposed to prevent restenosis following angioplasty or heart transplant vasculopathy.