Mitophagy in Huntington's disease

被引：29

作者：

Sonsky, I ^{[1
,2
]}

Vodicka, P. ^{[3
]}

Kepkova, K. Vodickova ^{[3
]}

Hansikova, H. ^{[1
,2
]}

机构：

[1] Charles Univ Prague, Fac Med 1, Dept Pediat & Inherited Metab Disorders, Lab Study Mitochondrial Disorders, Prague, Czech Republic

[2] Gen Univ Hosp Prague, Prague, Czech Republic

[3] Czech Acad Sci, Lab Appl Proteome Anal, Inst Anim Physiol & Genet, Libechov, Czech Republic

来源：

NEUROCHEMISTRY INTERNATIONAL | 2021年 / 149卷

关键词：

Mitochondria; Mitophagy; Huntington's disease; Mitophagy adaptors; Pharmacological induction of mitophagy; TRANSCRIPTION FACTOR NRF2; MUTANT-HUNTINGTIN; MITOCHONDRIAL FISSION; POLYGLUTAMINE EXPANSION; NEUROLOGICAL PHENOTYPE; SELECTIVE AUTOPHAGY; CARGO RECOGNITION; CAG REPEAT; CELL-DEATH; PROTEIN;

D O I：

10.1016/j.neuint.2021.105147

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Huntington's disease (HD), as well as Parkinson's disease and Alzheimer's disease, belong to a group of neurodegenerative diseases characterized by common features, such as the progressive loss of neurons and the presence of pathogenic forms of misfolded protein aggregates. A quality control system such as autophagy is crucial for the clearance of protein aggregates and dysfunctional organelles and thus essential for the maintenance of neuronal homeostasis. The constant high energy demand of neuronal tissue links neurodegeneration to mitochondria. Inefficient removal of damaged mitochondria is thought to contribute to the pathogenesis of neurodegenerative diseases such as HD. In addition, direct involvement of the huntingtin protein in the autophagic machinery has been described. In this review, we focus on mitophagy, a selective form of autophagy responsible for mitochondrial turnover. We also discuss the relevance of pharmacological regulation of mitophagy in the future therapeutic approach to neurodegenerations, including HD.

引用

页数：11

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