Abstract
Vascular calcification (VC) is an independent cardiovascular event and also a complication commonly found in chronic kidney disease (CKD) and diabetic patients. The mechanisms underpinning pathophysiology of VC is yet to be fully understood. Nevertheless, certain processes are generally believed to participate in its onset and progression. VC pathology is characterized by disequilibrium in the amount of natural inhibitors and active inducers of VC process. The imbalance may favor ectopic deposition of calcium-phosphate in form of hydroxyapatite in media or intima tunica compartments of blood vessels. This eventually could trigger phenotypic switch of smooth muscle cells to osteoblasts related cells. Thus, VSMC phenotypic trans-differentiation is currently considered as one of the hallmarks of VC. At the moment, there is no approved treatment. Fibroblast growth factors (FGFs) are a protein family that participates in varieties of biological processes. More recently, FGF21 seems to be gaining more attention with recent findings showing its anti-calcifying efficacy. In this review, the aim is to point out specific processes involved in VC and also to highlight the participation of FGF21 in the pathology of vascular calcification.