How Does Pink1 Repair Mitchondria

Review

. 2021 November four;10(11):3022.

doi: 10.3390/cells10113022.

Disruption of Mitochondrial Homeostasis: The Function of PINK1 in Parkinson'south Disease

Affiliations

PMID: 34831247
PMCID: PMC8616241
DOI: 10.3390/cells10113022

Free PMC article

Review

Disruption of Mitochondrial Homeostasis: The Function of PINK1 in Parkinson's Disease

Maria Vizziello et al. Cells. 2021 .

Free PMC article

Abstract

The progressive reduction of the dopaminergic neurons of the substantia nigra is the central procedure underlying Parkinson'southward affliction (PD), while the machinery of susceptibility of this specific neuronal population is largely unclear. Disturbances in mitochondrial role take been recognized every bit one of the chief pathways in sporadic PD since the finding of respiratory chain impairment in beast models of PD. Studies on genetic forms of PD have provided new insight on the role of mitochondrial bioenergetics, homeostasis, and autophagy. PINK1 (PTEN-induced putative kinase 1) gene mutations, although rare, are the 2nd near common cause of recessively inherited early-onset PD, after Parkin gene mutations. Our noesis of PINK1 and Parkin function has increased dramatically in the final years, with the discovery that a procedure chosen mitophagy, which plays a key office in the maintenance of mitochondrial health, is mediated by the PINK1/Parkin pathway. In vitro and in vivo models have been developed, supporting the office of PINK1 in synaptic manual, particularly affecting dopaminergic neurons. It is of paramount importance to further define the office of PINK1 in mitophagy and mitochondrial homeostasis in PD pathogenesis in order to delineate novel therapeutic targets.

Keywords: PINK1; Parkin; Parkinson's disease; mitochondrial quality control; mitophagy.

Conflict of interest argument

The authors declare no disharmonize of interest.

Figures

**Figure 1**
Domain compages of PINK1 (581 amino acids). Mitochondrial targeting sequence (MTS, orange), transmembrane domain (TMD, blue).

**Effigy 2**

Schematic representation of PINK1-Parkin mitochondrial centrality and some of the above-mentioned master potential therapeutic targets. PTEN-L, phosphate and tension homology deleted on chromosome 10-long; Ub, ubiquitin; USP, ubiquitin specific protease; NIX, Nip3-like protein 10; PARL, presenilins-associated rhomboid-like poly peptide. Created with
BioRender.com
.

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