Reactive Oxygen Species as Mediators of Signal Transduction in Ischemic Preconditioning

2004 ◽  
Vol 6 (2) ◽  
pp. 449-469 ◽  
Author(s):  
Hajime Otani
Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 963 ◽  
Author(s):  
Andrea Tóth ◽  
Enikő Balogh ◽  
Viktória Jeney

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.


2012 ◽  
Vol 2012 ◽  
pp. 1-22 ◽  
Author(s):  
Soumen Bhattacharjee

Reactive oxygen species (ROS) are astonishingly versatile molecular species and radicals that are poised at the core of a sophisticated network of signaling pathways of plants and act as core regulator of cell physiology and cellular responses to environment. ROS are continuously generated in plants as an inevitable consequence of redox cascades of aerobic metabolism. In one hand, plants are surfeited with the mechanism to combat reactive oxygen species, in other circumstances, plants appear to purposefully generate (oxidative burst) and exploit ROS or ROS-induced secondary breakdown products for the regulation of almost every aspect of plant biology, from perception of environmental cues to gene expression. The molecular language associated with ROS-mediated signal transduction, leading to modulation in gene expression to be one of the specific early stress response in the acclamatory performance of the plant. They may even act as “second messenger” modulating the activities of specific proteins or expression of genes by changing redox balance of the cell. The network of redox signals orchestrates metabolism for regulating energy production to utilization, interfering with primary signaling agents (hormones) to respond to changing environmental cues at every stage of plant development. The oxidative lipid peroxidation products and the resulting generated products thereof (associated with stress and senescence) also represent “biological signals,” which do not require preceding activation of genes. Unlike ROS-induced expression of genes, these lipid peroxidation products produce nonspecific response to a large variety of environmental stresses. The present review explores the specific and nonspecific signaling language of reactive oxygen species in plant acclamatory defense processes, controlled cell death, and development. Special emphasis is given to ROS and redox-regulated gene expression and the role of redox-sensitive proteins in signal transduction event. It also describes the emerging complexity of apparently contradictory roles that ROS play in cellular physiology to ascertain their position in the life of the plant.


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