Abstract
Vascular calcification is the deposition of hydroxyapatite crystals in the medial or intimal layers of arteries that is usually associated with other pathological conditions including but not limited to chronic kidney disease, atherosclerosis and diabetes. Calcification is an active, cell-regulated process involving the phenotype transition of vascular smooth muscle cells (VSMCs) from contractile to osteoblast/chondrocyte-like cells. Diverse triggers and signal transduction pathways have been identified behind vascular calcification. In this review, we focus on the role of reactive oxygen species (ROS) in the osteochondrogenic phenotype switch of VSMCs and subsequent calcification. Vascular calcification is associated with elevated ROS production. Excessive ROS contribute to the activation of certain osteochondrogenic signal transduction pathways, thereby accelerating osteochondrogenic transdifferentiation of VSMCs. Inhibition of ROS production and ROS scavengers and activation of endogenous protective mechanisms are promising therapeutic approaches in the prevention of osteochondrogenic transdifferentiation of VSMCs and subsequent vascular calcification. The present review discusses the formation and actions of excess ROS in different experimental models of calcification, and the potential of ROS-lowering strategies in the prevention of this deleterious condition.
Highlights
Ectopic calcification is the deposition of calcium (Ca) and phosphate (PO4 3−, P)-containing hydroxyapatite crystals in any soft tissue
Vascular calcification was considered as a degenerative passive process related to aging and increased concentrations of P and Ca, a notion which was supported by the observation that elderly people and chronic kidney disease (CKD) patients are the most affected ones [2]
A growing body of evidence suggests the contribution of reactive oxygen species (ROS) in osteochondrogenic signal transduction pathways, and the involvement of redox signaling in osteochondrogenic transdifferentiation of vascular smooth muscle cells (VSMCs) (Figure 3)
Summary
Ectopic calcification is the deposition of calcium (Ca) and phosphate (PO4 3− , P)-containing hydroxyapatite crystals in any soft tissue. Vascular smooth muscle cells (VSMCs) present in the media layer of vessels play a central role in vascular calcification. VSMCs undergo a phenotype switch, resulting in a cell type resembling osteoblasts or chondrocytes [9]. This phenotype switch is referred as osteochondrogenic transdifferentiation. Besides Pi, numerous triggers and inhibitors of such phenotype switching have been identified, and alterations in the balance of these pro- and anti-calcific stimuli are considered to eventually lead to ectopic mineral deposition [12]. Accumulating evidence suggests that (i) vascular calcification is associated with elevated ROS production, and (ii) excess ROS play a pathophysiological role in the process of vascular calcification. We aim to summarize our current knowledge about the involvement of ROS in the development of vascular calcification
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