PINK1/Parkin Mediated Mitophagy, Ca2+ Signalling, and ER-Mitochondria Contacts in Parkinson's Disease

被引：149

作者：

Barazzuol, Lucia ^{[1
]}

Giamogante, Flavia ^{[1
]}

Brini, Marisa ^{[2
]}

Cali, Tito ^{[1
,3
]}

机构：

[1] Univ Padua, Dept Biomed Sci, I-35131 Padua, Italy

[2] Univ Padua, Dept Biol, I-35131 Padua, Italy

[3] Univ Padua, PNC, I-35131 Padua, Italy

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2020年 / 21卷 / 05期

关键词：

PINK1; Parkin; mitophagy; Ca2+; ER-mitochondria tethering; ENDOPLASMIC-RETICULUM; PINK1-DEPENDENT PHOSPHORYLATION; PATHOPHYSIOLOGICAL ROLES; REGULATES MITOPHAGY; CALCIUM HOMEOSTASIS; UBIQUITIN CHAIN; PINK1; AUTOPHAGY; E3; DEGRADATION;

D O I：

10.3390/ijms21051772

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：

Endoplasmic reticulum (ER)-mitochondria contact sites are critical structures for cellular function. They are implicated in a plethora of cellular processes, including Ca2+ signalling and mitophagy, the selective degradation of damaged mitochondria. Phosphatase and tensin homolog (PTEN)-induced kinase (PINK) and Parkin proteins, whose mutations are associated with familial forms of Parkinson's disease, are two of the best characterized mitophagy players. They accumulate at ER-mitochondria contact sites and modulate organelles crosstalk. Alterations in ER-mitochondria tethering are a common hallmark of many neurodegenerative diseases including Parkinson's disease. Here, we summarize the current knowledge on the involvement of PINK1 and Parkin at the ER-mitochondria contact sites and their role in the modulation of Ca2+ signalling and mitophagy.

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页数：17

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