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已发表论文
尿酸肾病中线粒体氧化应激与血管重塑：机制见解及治疗意义
Authors Liang J, Qiu Y, Fu T, Li J, Xiao F, Xing G, Cai H, Tong Y
Received 25 June 2025
Accepted for publication 24 September 2025
Published 29 September 2025 Volume 2025:18 Pages 281—301
DOI https://doi.org/10.2147/IJNRD.S549209
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Professor Pravin Singhal
Jiahao Liang,1 Yanzhi Qiu,1 Tong Fu,2 Jianing Li,1 Fei Xiao,1 Guoli Xing,1 Hongbo Cai,1 Ying Tong1
1Graduate School, Heilongjiang University of Chinese Medicine, Harbin, People’s Republic of China; 2Department of Psychology, Brandeis University, Waltham, MA, USA
Correspondence: Ying Tong, Email tongying@hljucm.edu.cn
Abstract: Uric acid nephropathy (UAN), driven by sustained hyperuricemia, is an underrecognized but increasingly prevalent contributor to chronic kidney disease (CKD) progression. Mitochondrial oxidative stress and vascular remodeling are central to its pathogenesis. Excess mitochondrial reactive oxygen species (ROS) cause renal tubular injury, impair mitophagy, and activate pro-apoptotic signaling pathways. In parallel, ROS disrupt endothelial homeostasis, promote phenotypic switching of vascular smooth muscle cells, and induce pathological structural changes in the renal microvasculature. These processes are mutually reinforcing, thereby exacerbating inflammation, hypoxia, and fibrosis. This review synthesizes emerging mechanistic insights into the mitochondrial–vascular axis in UAN and discusses therapeutic strategies targeting mitochondrial dysfunction and vascular pathology. Particular emphasis is placed on mitochondria-targeted antioxidants and inhibitors of key signaling pathways as potential interventions to interrupt the ROS–remodeling cycle. We also highlight the need for biomarker development and clinical translation. A more comprehensive understanding of mitochondrial–vascular crosstalk may ultimately enable the development of effective strategies to slow or halt UAN progression.
Keywords: uric acid nephropathy, mitochondrial dysfunction, oxidative stress, vascular remodeling, reactive oxygen species, endothelial dysfunction, mitochondria-targeted therapy
1Graduate School, Heilongjiang University of Chinese Medicine, Harbin, People’s Republic of China; 2Department of Psychology, Brandeis University, Waltham, MA, USA
Correspondence: Ying Tong, Email tongying@hljucm.edu.cn
Abstract: Uric acid nephropathy (UAN), driven by sustained hyperuricemia, is an underrecognized but increasingly prevalent contributor to chronic kidney disease (CKD) progression. Mitochondrial oxidative stress and vascular remodeling are central to its pathogenesis. Excess mitochondrial reactive oxygen species (ROS) cause renal tubular injury, impair mitophagy, and activate pro-apoptotic signaling pathways. In parallel, ROS disrupt endothelial homeostasis, promote phenotypic switching of vascular smooth muscle cells, and induce pathological structural changes in the renal microvasculature. These processes are mutually reinforcing, thereby exacerbating inflammation, hypoxia, and fibrosis. This review synthesizes emerging mechanistic insights into the mitochondrial–vascular axis in UAN and discusses therapeutic strategies targeting mitochondrial dysfunction and vascular pathology. Particular emphasis is placed on mitochondria-targeted antioxidants and inhibitors of key signaling pathways as potential interventions to interrupt the ROS–remodeling cycle. We also highlight the need for biomarker development and clinical translation. A more comprehensive understanding of mitochondrial–vascular crosstalk may ultimately enable the development of effective strategies to slow or halt UAN progression.
Keywords: uric acid nephropathy, mitochondrial dysfunction, oxidative stress, vascular remodeling, reactive oxygen species, endothelial dysfunction, mitochondria-targeted therapy