Redox signaling, Nox5 and vascular remodeling in hypertension
Autor: | Montezano, Augusto C., Tsiropoulou, Sofia, Dulak-Lis, Maria, Harvey, Adam, De Lucca Camargo, Livia, Touyz, Rhian M. |
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Jazyk: | angličtina |
Rok vydání: | 2015 |
Předmět: |
reactive oxygen species
NADPH oxidase oxidative post-translational modification Membrane Proteins NADPH Oxidases Vascular Remodeling NADPH Oxidase 5 PHARMACOLOGY AND THERAPEUTICS: Edited by Adam Whaley-Connell and C. John Sperati Hypertension vascular smooth muscle cells Animals Humans Oxidation-Reduction Signal Transduction |
Zdroj: | Current Opinion in Nephrology and Hypertension |
ISSN: | 1062-4821 |
Popis: | Purpose of review: Extensive data indicate a role for reactive oxygen species (ROS) and redox signaling in vascular damage in hypertension. However, molecular mechanisms underlying these processes remain unclear, but oxidative post-translational modification of vascular proteins is critical. This review discusses how proteins are oxidatively modified and how redox signaling influences vascular smooth muscle cell growth and vascular remodeling in hypertension. We also highlight Nox5 as a novel vascular ROS-generating oxidase.\ud Recent findings: Oxidative stress in hypertension leads to oxidative imbalance that affects vascular cell function through redox signaling. Many Nox isoforms produce ROS in the vascular wall, and recent findings show that Nox5 may be important in humans. ROS regulate signaling by numerous processes including cysteine oxidative post-translational modification such as S-nitrosylation, S-glutathionylation and sulfydration. In vascular smooth muscle cells, this influences cellular responses to oxidative stimuli promoting changes from a contractile to a proliferative phenotype.\ud Summary: In hypertension, Nox-induced ROS production is increased, leading to perturbed redox signaling through oxidative modifications of vascular proteins. This influences mitogenic signaling and cell cycle regulation, leading to altered cell growth and vascular remodeling in hypertension. |
Databáze: | OpenAIRE |
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