Regulation of Vascular Calcification by Reactive Oxygen Species

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...

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Bibliographic Details
Published in:Antioxidants 2020-10, Vol.9 (10), p.963
Main Authors: Tóth, Andrea, Balogh, Enikő, Jeney, Viktória
Format: Article
Language:English
Subjects:
Arteries
Arteriosclerosis
Atherosclerosis
Calcification
Calcification (ectopic)
Cardiovascular disease
Chondrocytes
Crystals
Diabetes
Diabetes mellitus
Genotype & phenotype
Health aspects
Homeostasis
Hydroxyapatite
Hypertension
Kidney diseases
Mineralization
Mortality
Muscle cells
Muscle contraction
osteochondrogenic transdifferentiation
Oxidative stress
Phenotypes
Proteins
Reactive oxygen species
reactive oxygen species (ROS)
Review
Runx2
Signal transduction
Smooth muscle
Stem cells
Transcription factors
Tumor necrosis factor-TNF
vascular calcification
vascular smooth muscle cells (VSMCs)
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Summary: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.
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox9100963