The Role of the PINK1-Parkin Pathway in Mitophagy and Its Implications in Neurodegenerative Disorders

Abstract

Mitochondria play a crucial role in cellular biological energy production, regulation of reactive oxygen species, and the synthesis of biological macromolecules. Mitophagy, on the other hand, is responsible for the selective degradation of damaged mitochondria and serves as a vital cellular process for maintaining neuronal homeostasis. Dysfunctional mitophagy leads to a disruption in mitochondrial quality control, which can result in or exacerbate neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, and Huntington's disease. The PINK1/Parkin pathway initiates mitophagy through a series of ubiquitin-mediated signaling events in response to mitochondrial damage, promoting the degradation of impaired mitochondria. Disruption of this pathway leads to mitochondrial dysfunction, energy imbalance, oxidative stress, and neuronal degeneration, which are hallmark features of neurodegenerative diseases. Furthermore, impaired mitophagy has been shown to contribute to the pathogenesis of these disorders. In this review, we examine the molecular mechanisms of mitophagy, particularly the PINK1/Parkin pathway, and explore its effects on neurodegenerative diseases.

Cite this article as: Sever T, Erbaş O. The Role of the PINK1-Parkin Pathway in Mitophagy and Its Implications in Neurodegenerative Disorders. JEB Med Sci 2024;5(4):264-270.

The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.

The authors received no financial support for the research and/or authorship of this article.