The hallmarks of mitochondrial dysfunction in chronic kidney disease

被引:346
作者
Galvan, Daniel L. [1 ]
Green, Nathanael H. [2 ]
Danesh, Farhad R. [1 ,2 ]
机构
[1] Univ Texas MD Anderson Canc Ctr, Nephrol Sect, 1400 Pressler St,Unit 1468, Houston, TX 77030 USA
[2] Baylor Coll Med, Dept Pharmacol & Chem Biol, Houston, TX 77030 USA
关键词
acute kidney injury; chronic kidney disease; diabetes; diabetic nephropathy; mitochondria; oxidative stress; DEPENDENT PROTEIN-KINASE; DIABETIC-NEPHROPATHY; RECEPTOR-GAMMA; RENAL-DISEASES; PODOCYTES; INJURY; PHOSPHORYLATION; FISSION; DRP1; COACTIVATOR;
D O I
10.1016/j.kint.2017.05.034
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Recent advances have led to a greater appreciation of how mitochondrial dysfunction contributes to diverse acute and chronic pathologies. Indeed, mitochondria have received increasing attention as a therapeutic target in a variety of diseases because they serve as key regulatory hubs uniquely situated at crossroads between multiple cellular processes. This review provides an overview of the role of mitochondrial dysfunction in chronic kidney disease, with special emphasis on its role in the development of diabetic nephropathy. We examine the current understanding of the molecular mechanisms that cause mitochondrial dysfunction in the kidney and describe the impact of mitochondrial damage on kidney function. The new concept that mitochondrial shape and structure are closely linked with its function in the kidneys is discussed. Furthermore, the mechanisms that translate cellular cues and demands into mitochondrial remodeling and cellular damage, including the role of microRNAs and long noncoding RNAs, are examined with the final goal of identifying mitochondrial targets to improve treatment of patients with chronic kidney diseases.
引用
收藏
页码:1051 / 1057
页数:7
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