Mitochondria and vascular calcification in chronic kidney disease: Lessons learned from the past to improve future therapy

J Cell Physiol. 2022 Dec;237(12):4369-4396. doi: 10.1002/jcp.30891. Epub 2022 Oct 2.

Abstract

Chronic kidney disease-mineral and bone disorders (CKD-MBD) is a common complication of CKD Stages 3-5. Hyperphosphatemia is one of the major metabolic components of CKD-MBD, frequently resulting in vascular calcification (VC) in advanced-stage patients. Also, a long duration of renal replacement therapy can cause the worsening of VC, leading to increased cardiovascular morbidity and mortality. Vascular smooth muscle cells play an important role in the development of VC through osteochondrogenic transformation and the apoptotic process. It has been shown that mitochondrial dysfunction is involved with CKD progression, and excessive oxidative stress can aggravate osteoblastic transformation and VC. Currently, novel interventions targeting mitochondrial function and dynamics, in addition to mitochondrial antioxidants, have been studied with the aim of attenuating VC. This review aims to comprehensively summarize and discuss the experimental and clinical reports concerning mitochondrial studies, along with the purpose of interventions that can improve the outcomes of VC among CKD patients.

Keywords: CKD-MBD; chronic kidney disease; mitochondria; osteochondrogenic transformation; vascular calcification.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Chronic Kidney Disease-Mineral and Bone Disorder* / complications
  • Humans
  • Hyperphosphatemia* / etiology
  • Hyperphosphatemia* / metabolism
  • Mitochondria* / metabolism
  • Mitochondria* / pathology
  • Renal Insufficiency, Chronic* / complications
  • Renal Insufficiency, Chronic* / metabolism
  • Vascular Calcification* / etiology
  • Vascular Calcification* / metabolism