Camargo Livia L, Rios Francisco J, Montezano Augusto C, Touyz Rhian M
Research Institute of the McGill University Health Centre (RI-MUHC), Montreal, Quebec, Canada.
Department of Medicine, Faculty of Medicine and Health Sciences, McGill University, Montreal, Quebec, Canada.
Nat Rev Cardiol. 2025 Jan;22(1):20-37. doi: 10.1038/s41569-024-01062-6. Epub 2024 Jul 24.
Hypertension is a leading risk factor for stroke, heart disease and chronic kidney disease. Multiple interacting factors and organ systems increase blood pressure and cause target-organ damage. Among the many molecular elements involved in the development of hypertension are reactive oxygen species (ROS), which influence cellular processes in systems that contribute to blood pressure elevation (such as the cardiovascular, renal, immune and central nervous systems, or the renin-angiotensin-aldosterone system). Dysregulated ROS production (oxidative stress) is a hallmark of hypertension in humans and experimental models. Of the many ROS-generating enzymes, NADPH oxidases are the most important in the development of hypertension. At the cellular level, ROS influence signalling pathways that define cell fate and function. Oxidative stress promotes aberrant redox signalling and cell injury, causing endothelial dysfunction, vascular damage, cardiovascular remodelling, inflammation and renal injury, which are all important in both the causes and consequences of hypertension. ROS scavengers reduce blood pressure in almost all experimental models of hypertension; however, clinical trials of antioxidants have yielded mixed results. In this Review, we highlight the latest advances in the understanding of the role and the clinical implications of ROS in hypertension. We focus on cellular sources of ROS, molecular mechanisms of oxidative stress and alterations in redox signalling in organ systems, and their contributions to hypertension.
高血压是中风、心脏病和慢性肾病的主要危险因素。多种相互作用的因素和器官系统会升高血压并导致靶器官损害。参与高血压发生发展的众多分子因素中，活性氧（ROS）会影响导致血压升高的系统（如心血管、肾脏、免疫和中枢神经系统，或肾素-血管紧张素-醛固酮系统）中的细胞过程。活性氧生成失调（氧化应激）是人类和实验模型中高血压的一个标志。在众多产生活性氧的酶中，NADPH氧化酶在高血压的发生发展中最为重要。在细胞水平上，活性氧影响决定细胞命运和功能的信号通路。氧化应激促进异常的氧化还原信号传导和细胞损伤，导致内皮功能障碍、血管损伤、心血管重塑、炎症和肾损伤，这些在高血压的病因和后果中都很重要。活性氧清除剂在几乎所有高血压实验模型中都能降低血压；然而，抗氧化剂的临床试验结果不一。在本综述中，我们重点介绍了对活性氧在高血压中的作用及临床意义的最新认识进展。我们关注活性氧的细胞来源、氧化应激的分子机制以及器官系统中氧化还原信号的改变，及其对高血压的影响。
