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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| Format: | Article |
| Language: | English |
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MDPI AG
2020-10-01
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| Series: | Antioxidants |
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| Online Access: | https://www.mdpi.com/2076-3921/9/10/963 |
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| author | Andrea Tóth Enikő Balogh Viktória Jeney |
| author_facet | Andrea Tóth Enikő Balogh Viktória Jeney |
| author_sort | Andrea Tóth |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-03-10T15:46:48Z |
| format | Article |
| id | doaj.art-8359874161994749a91d13bebcabba0d |
| institution | Directory Open Access Journal |
| issn | 2076-3921 |
| language | English |
| last_indexed | 2024-03-10T15:46:48Z |
| publishDate | 2020-10-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Antioxidants |
| spelling | doaj.art-8359874161994749a91d13bebcabba0d2023-11-20T16:21:25ZengMDPI AGAntioxidants2076-39212020-10-0191096310.3390/antiox9100963Regulation of Vascular Calcification by Reactive Oxygen SpeciesAndrea Tóth0Enikő Balogh1Viktória Jeney2MTA-DE Lendület Vascular Pathophysiology Research Group, Research Centre for Molecular Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, HungaryMTA-DE Lendület Vascular Pathophysiology Research Group, Research Centre for Molecular Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, HungaryMTA-DE Lendület Vascular Pathophysiology Research Group, Research Centre for Molecular Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, HungaryVascular 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.https://www.mdpi.com/2076-3921/9/10/963vascular calcificationreactive oxygen species (ROS)vascular smooth muscle cells (VSMCs)osteochondrogenic transdifferentiationRunx2 |
| spellingShingle | Andrea Tóth Enikő Balogh Viktória Jeney Regulation of Vascular Calcification by Reactive Oxygen Species Antioxidants vascular calcification reactive oxygen species (ROS) vascular smooth muscle cells (VSMCs) osteochondrogenic transdifferentiation Runx2 |
| title | Regulation of Vascular Calcification by Reactive Oxygen Species |
| title_full | Regulation of Vascular Calcification by Reactive Oxygen Species |
| title_fullStr | Regulation of Vascular Calcification by Reactive Oxygen Species |
| title_full_unstemmed | Regulation of Vascular Calcification by Reactive Oxygen Species |
| title_short | Regulation of Vascular Calcification by Reactive Oxygen Species |
| title_sort | regulation of vascular calcification by reactive oxygen species |
| topic | vascular calcification reactive oxygen species (ROS) vascular smooth muscle cells (VSMCs) osteochondrogenic transdifferentiation Runx2 |
| url | https://www.mdpi.com/2076-3921/9/10/963 |
| work_keys_str_mv | AT andreatoth regulationofvascularcalcificationbyreactiveoxygenspecies AT enikobalogh regulationofvascularcalcificationbyreactiveoxygenspecies AT viktoriajeney regulationofvascularcalcificationbyreactiveoxygenspecies |