Oxidative phosphorylation promotes vascular calcification in chronic kidney disease |
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| Authors: | Jia Shi Yi Yang Ya-Nan Wang Qing Li Xue Xing An-Ying Cheng Xiao-Na Zhan Jie Li Gang Xu Fan He |
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| Affiliation: | Department of Nephrology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1095 Wuhan, Jiefang Ave China |
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| Abstract: | Metabolism has been reported to associate with the progression of vascular diseases. However, how vascular calcification in chronic kidney disease (CKD) is regulated by metabolic status remains poorly understood. Using a model of 5/6 nephrectomy, we demonstrated that the aortic tissues of CKD mice had a preference for using oxidative phosphorylation (OXPHOS). Both high phosphate and human uremic serum-stimulated vascular smooth muscle cells (VSMCs) had enhanced mitochondrial respiration capacity, while the glycolysis level was not significantly different. Besides, 2-deoxy-d-glucose (2-DG) exacerbated vascular calcification by upregulating OXPHOS. The activity of cytochrome c oxidase (COX) was higher in the aortic tissue of CKD mice than those of sham-operated mice. Moreover, the expression levels of COX15 were higher in CKD patients with aortic arch calcification (AAC) than those without AAC, and the AAC scores were correlated with the expression level of COX15. Suppressing COX sufficiently attenuated vascular calcification. Our findings verify the relationship between OXPHOS and calcification, and may provide potential therapeutic approaches for vascular calcification in CKD.Subject terms: Calcification, End-stage renal disease |
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