Central role of c-Src in NOX5- mediated redox signaling in vascular smooth muscle cells in human hypertension

CONCLUSIONS: We define NOX5/ROS/c-Src as a novel feedforward signaling network in human VSMCs. Amplification of this system in hypertension contributes to VSMC dysfunction. Dampening the NOX5/ROS/c-Src pathway may ameliorate hypertension-associated vascular injury.TRANSLATIONAL PERSPECTIVE: Oxidative stress is a major factor contributing to vascular damage in hypertension. We corroborate experimental evidence that NOX-derived ROS generation is increased in human vascular smooth muscle cells (VSMC) and demonstrate that in human hypertension NOX5 upregulation is a major trigger of VSMC dysfunction. We uncover new regulatory molecular mechanisms of NOX5 and define NOX5/ROS/c-Src as a novel signaling pathway in human VSMCs. This system is augmented in hypertension contributing to abnormal VSMC redox signaling, cytoskeletal disorganization and vascular dysfunction. Modulating the NOX5/ROS/c-Src pathway may have therapeutic potential by targeting redox signaling pathways involved in vascular dysfunction associated with hypertension.PMID:34320175 | DOI:10.1093/cvr/cvab171

Source: Cell Research - July 28, 2021 Category: Cytology Authors: Livia L Camargo Augusto C Montezano Misbah Hussain Yu Wang Zhiguo Zou Francisco J Rios Karla B Neves Rheure Alves-Lopes Fazli R Awan Tomasz J Guzik Thomas Jensen Richard C Hartley Rhian M Touyz Source Type: research