The Role of Mitochondrial Dysfunction in CKD-Related Vascular Calcification: From Mechanisms to Therapeutics

作者：Junmin Huang, Junfeng Hao, Peng Wang, Yongzhi Xu · 发表于：Kidney International Reports · 年份：2024 · DOI：10.1016/j.ekir.2024.05.005 · 被引用次数：16 · 研究领域：Parathyroid Disorders and Treatments、Medical Imaging and Pathology Studies、Heterotopic Ossification and Related Conditions

Vascular calcification (VC) is a common complication of chronic kidney disease (CKD) and is closely associated with cardiovascular events. The transdifferentiation of vascular smooth muscles (VSMCs) into an osteogenic phenotype is hypothesized to be the primary cause underlying VC. However, there is currently no effective clinical treatment for VC. Growing evidence suggests that mitochondrial dysfunction accelerates the osteogenic differentiation of VSMCs and VC via multiple mechanisms. Therefore, elucidating the relationship between the osteogenic differentiation of VSMCs and mitochondrial dysfunction may assist in improving VC-related adverse clinical outcomes in patients with CKD. This review aimed to summarize the role of mitochondrial biogenesis, mitochondrial dynamics, mitophagy, and metabolic reprogramming, as well as mitochondria-associated oxidative stress (OS) and senescence in VC in patients with CKD to offer valuable insights into the clinical treatment of VC.