Backston Kyle, Morgan Jordan, Patel Samipa, Koka Riddhima, Hu Jieji, Raina Rupesh
College of Medicine, Northeast Ohio Medical University, Rootstown, OH 44272, USA.
Solon High School, Solon, OH 44139, USA.
Int J Mol Sci. 2025 Jun 3;26(11):5355. doi: 10.3390/ijms26115355.
Pediatric hypertension is increasingly recognized as a complex condition shaped by both systemic and cellular factors, with oxidative stress emerging as a key driver of vascular dysfunction. In both their primary and secondary forms, reactive oxygen species (ROS) disrupt redox homeostasis, impair endothelial signaling, and promote inflammation and tissue remodeling. Metabolic dysregulation, renal pathology, and early-life stressors contribute to the accumulation of ROS through pathways involving NADPH oxidases, mitochondrial dysfunction, xanthine oxidase activity, and altered arginine metabolism. These mechanisms converge on the vasculature, diminishing nitric oxide bioavailability and promoting hypertensive phenotypes. Beyond disease initiation, redox imbalance influences the response to treatment, surgical outcomes, and long-term cardiovascular risk. By further elucidating these mechanisms, the complex relationship between oxidative stress, vascular biology, and blood pressure regulation in children may be more clearly defined and more effectively targeted in clinical management.
小儿高血压日益被视为一种由全身和细胞因素共同塑造的复杂病症，氧化应激已成为血管功能障碍的关键驱动因素。在原发性和继发性形式中，活性氧（ROS）都会破坏氧化还原稳态，损害内皮信号传导，并促进炎症和组织重塑。代谢失调、肾脏病理以及早期生活应激源通过涉及烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶、线粒体功能障碍、黄嘌呤氧化酶活性和精氨酸代谢改变的途径导致ROS积累。这些机制作用于血管系统，降低一氧化氮的生物利用度并促进高血压表型。除了疾病的起始阶段，氧化还原失衡还会影响治疗反应、手术结果和长期心血管风险。通过进一步阐明这些机制，儿童氧化应激、血管生物学和血压调节之间的复杂关系可能会在临床管理中得到更清晰的界定和更有效的针对性治疗。
