ATHEROSCLEROSIS, VASCULAR CALCIFICATION AND BONE LOSS (OSTEOPOROSIS): COMMON PATHOPHYSIOLOGICAL MRCHANISMS DEVELOPMENT OF THE DESEASES AND RESEARCH NOVEL DRAGS FOR DUAL THERAPIE

Abstract

Atherosclerosis and osteoporosis are public health problems, with several epidemiological links, and they might be related to each other in terms of pathogenesis and therapeutic agents. The correlation between atherosclerosis and osteoporosis is being established by studies of the underling pathophysiological mechanisms, which seem to coincide in many biochemical pathways, and of the risk factors for vascular disease, which have also been associated with a higher incidence of low bone mineral density. Many experiments showing that the receptor activator of NF-kB (RANK), its ligand (RANKL), and the decoy osteoprotegerin receptor (OPG) are essential, central regulators of bone metabolism were significant turning points in our understanding of bone disease. Moreover, one emerging area in vascular biology involves the RANKL-RANK-OPG system, molecules of the tumor necrosis factor-related family recently discovered to be critical regulators of vessels calcification process. Animal and human studies results confirm the RANKL-RANK-OPG role in pathogenesis of vascular calcification and osteoporosis. Thus, these molecules may play a central role in regulation the development of vascular calcification coincident with declines in skeletal mineralization. Understanding cellular and molecular mechanisms of vascular calcification and osteoporosis may potentially lead to therapeutic opportunities for treating people with osteoporosis and cardiovascular diseases.

Keywords

• rank-rankl-opg система
• atherosclerosis
• osteoporosis
• common mechanisms
• rankl-rank-opg system
• cathepsin k
• denosumab
• odanacatib