Mitochondrial Dysfunction: Cause or Consequence of Vascular Calcification?

被引:51
|
作者
Phadwal, Kanchan [1 ,2 ]
Vrahnas, Christina [3 ]
Ganley, Ian G. [3 ]
MacRae, Vicky E. [1 ,2 ]
机构
[1] Univ Edinburgh, Roslin Inst, Funct Genet & Dev Div, Edinburgh, Midlothian, Scotland
[2] Univ Edinburgh, Royal Dick Sch Vet Studies, Edinburgh, Midlothian, Scotland
[3] Univ Dundee, Sir James Black Ctr, Med Res Council MRC Prot Phosphorylat & Ubiquityl, Dundee, Scotland
来源
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY | 2021年 / 9卷
基金
英国医学研究理事会; 英国生物技术与生命科学研究理事会;
关键词
mitochondria; VSMCs; calcification; mitophagy; oxidative phoshorylation; SMOOTH-MUSCLE-CELLS; GLYCATION END-PRODUCTS; GILFORD PROGERIA SYNDROME; GENERALIZED ARTERIAL CALCIFICATION; ELECTRON-MICROSCOPY REVEALS; TRANSCRIPTION FACTOR RUNX2; OXIDATIVE STRESS; AORTIC-VALVE; PYRUVATE-DEHYDROGENASE; EXTRACELLULAR-MATRIX;
D O I
10.3389/fcell.2021.611922
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mitochondria are crucial bioenergetics powerhouses and biosynthetic hubs within cells, which can generate and sequester toxic reactive oxygen species (ROS) in response to oxidative stress. Oxidative stress-stimulated ROS production results in ATP depletion and the opening of mitochondrial permeability transition pores, leading to mitochondria dysfunction and cellular apoptosis. Mitochondrial loss of function is also a key driver in the acquisition of a senescence-associated secretory phenotype that drives senescent cells into a pro-inflammatory state. Maintaining mitochondrial homeostasis is crucial for retaining the contractile phenotype of the vascular smooth muscle cells (VSMCs), the most prominent cells of the vasculature. Loss of this contractile phenotype is associated with the loss of mitochondrial function and a metabolic shift to glycolysis. Emerging evidence suggests that mitochondrial dysfunction may play a direct role in vascular calcification and the underlying pathologies including (1) impairment of mitochondrial function by mineral dysregulation i.e., calcium and phosphate overload in patients with end-stage renal disease and (2) presence of increased ROS in patients with calcific aortic valve disease, atherosclerosis, type-II diabetes and chronic kidney disease. In this review, we discuss the cause and consequence of mitochondrial dysfunction in vascular calcification and underlying pathologies; the role of autophagy and mitophagy pathways in preventing mitochondrial dysfunction during vascular calcification and finally we discuss mitochondrial ROS, DRP1, and HIF-1 as potential novel markers and therapeutic targets for maintaining mitochondrial homeostasis in vascular calcification.
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页数:17
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