摘要
Hyperphosphataemia is a key contributor to oxidative stress (OS) and cellular dysfunction across various pathological conditions. While numerous studies have associated phosphate overload with redox imbalances, the role of NADPH oxidase (NOX) in this process has received limited attention. NOX enzymes are major enzymatic sources of reactive oxygen species (ROS), and their activation has been implicated in the progression of chronic kidney disease, vascular calcification, metabolic disorders, and cancer development. Under hyperphosphataemic conditions, excessive ROS production exacerbates endothelial dysfunction, promotes vascular smooth muscle cell transdifferentiation, induces chronic inflammation, and facilitates tumour progression. Despite increasing evidence linking phosphate metabolism to NOX activation, the underlying molecular mechanisms remain poorly characterised. This review critically examines the relationship between hyperphosphataemia and NADPH oxidase-mediated OS and explores its impact on disease pathophysiology. By providing an integrated analysis of the current findings, this work aims to highlight the pathological consequences of phosphate-induced OS and identify potential therapeutic strategies to mitigate its effects.
摘要译文
高磷脂血症是氧化应激（OS）和细胞功能障碍在各种病理条件下的关键因素。尽管许多研究与氧化还原失衡有关，但NADPH氧化酶（NOX）在此过程中的作用受到了有限的关注。NOX酶是活性氧（ROS）的主要酶源，其激活与慢性肾脏疾病，血管钙化，代谢性疾病和癌症发育的进展有关。在高磷脂条件下，过度的ROS产生加剧了内皮功能障碍，促进血管平滑肌细胞转变，诱导慢性炎症并促进肿瘤的进展。尽管有越来越多的证据将磷酸盐代谢与NOX激活联系起来，但潜在的分子机制的表征仍然很差。这篇综述批判性地研究了高磷酸血症与NADPH氧化酶介导的OS之间的关系，并探讨了其对疾病病理生理学的影响。通过对当前发现的综合分析，这项工作旨在突出磷酸盐诱导的OS的病理后果，并确定潜在的治疗策略来减轻其影响。
Marco Antonio Lacerda-Abreu [1];José Roberto Meyer-Fernandes [2];. Hyperphosphataemia and NADPH Oxidase Regulation in Pathophysiological Processes: Implications for Oxidative Stress and Disease Progression[J]. Antioxidants, 2025,14(4): 461