2016年12月12日
PINK1 signaling in mitochondrial homeostasis and in aging (Review).
International Journal of Molecular Medicine
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- 巻
- Vol.39
- 号
- No.1
- 開始ページ
- 3
- 終了ページ
- 8
- 記述言語
- 英語
- 掲載種別
- 記事・総説・解説・論説等(学術雑誌)
- DOI
- 10.3892/ijmm.2016.2827
Mitochondrial dysfunction is involved in the pathology of Parkinson's disease, an age-associated neurodegenerative disorder. Phosphatase and tensin homolog (PTEN)-induced putative kinase protein 1 (PINK1) is responsible for the most common form of recessive Parkinson's disease. PINK1 is a mitochondrial kinase that is involved in mitrochondrial quality control and promotes cell survival. PINK1 has been shown to protect against neuronal cell death induced by oxidative stress. Accordingly, PINK1 deficiency is associated with mitochondrial dysfunction as well as increased oxidative cellular stress and subsequent neuronal cell death. In addition, several mitochondrial chaperone proteins have been shown to be substrates of the PINK1 kinase. In this review, we discuss recent studies concerning the signaling cascades and molecular mechanisms involved in the process of mitophagy, which is implicated in neurodegeneration and in related aging associated with oxidative stress. Particular attention will be given to the molecular mechanisms proposed to explain the effects of natural compounds and/or food ingredients against oxidative stress. Knowledge of the molecular mechanisms involved in this cellular protection could be critical for developing treatments to prevent and control excessive progression of neurodegenerative disorders.
- リンク情報
- ID情報
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- DOI : 10.3892/ijmm.2016.2827
- ISSN : 1791-244X
- PubMed ID : 27959386
- SCOPUS ID : 85007610472