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Editorial
. 2017 Feb 27:4:17.
doi: 10.21037/sci.2017.02.07. eCollection 2017.

Inappropriate trafficking of damaged mitochondria in Parkinson's disease

Chi-Jing Choong  1 , Hideki Mochizuki  1
Affiliations
Editorial

Inappropriate trafficking of damaged mitochondria in Parkinson's disease

Chi-Jing Choong et al. Stem Cell Investig. .
No abstract available

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Conflict of interest statement

Conflicts of Interest: The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Relationship of LRRK2 and PINK1/Parkin with Miro in mitochondrial transport and mitophagy. (A) LRRK2 forms a complex with Miro and promotes its removal from OMM. (B) PINK1 and Parkin associate with Miro on depolarized mitochondria. Phosphorylation of Miro by PINK1 activates proteasomal degradation of Miro through a Parkin-dependent mechanism. Destruction of Miro detaches damaged mitochondria from microtubule network. Mitochondria lose motility, leading to subsequent mitochondrial clearance. LRRK2 and PINK1/Parkin pathway function in parallel and converge on Miro. (C) By loss of function, mutations in LRRK2, Parkin or PINK1 disrupt interaction with Miro on damaged mitochondria and slow initiation of mitophagy. Abnormal swollen mitochondria and oxidative stresses accumulate, eventually leading to cell death.
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