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001-es BibID:BIBFORM089746
035-os BibID:(cikkazonosító)963
Első szerző:Tóth Andrea (molekuláris biológus)
Cím:Regulation of Vascular Calcification by Reactive Oxygen Species / Tóth Andrea, Balogh Enikő, Jeney Viktória
Dátum:2020
ISSN:2076-3921
Megjegyzések: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.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
vascular calcification
reactive oxygen species (ROS)
vascular smooth muscle cells (VSMCs)
osteochondrogenic transdifferentiation
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Megjelenés:Antioxidants. - 9 : 10 (2020), p. 1-24. -
További szerzők:Balogh Enikő (1987-) (molekuláris biológus) Jeney Viktória (1971-) (vegyész, kémia tanár)
Pályázati támogatás:K131535
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