# A central role for PINK1 in governing local mitochondrial biogenesis and degradation in neurons

**Authors:** Marlena Helms, Angelika B. Harbauer

PMC · DOI: 10.1007/s00018-025-06054-4 · 2026-01-12

## TL;DR

This review highlights how PINK1 helps maintain healthy mitochondria in neurons by regulating their creation and removal.

## Contribution

The paper emphasizes PINK1's role in local mitochondrial biogenesis and degradation in neurons.

## Key findings

- PINK1 is crucial for local mitochondrial biogenesis in neurons.
- PINK1 regulates mitochondrial degradation through proteases and mitophagy.
- PINK1 mRNA associates with mitochondria to maintain local function.

## Abstract

Neurons have adapted the transport and positioning of mitochondria to fit their extended shape and high energy needs. To sustain mitochondrial function, neurons developed systems that allow local biogenesis and adaption to locally regulate mitochondrial form and function. Likewise, fine-tuned degradative systems are required to protect the neurons from mitochondrial dysfunction. Throughout both domains of mitostasis, the local synthesis of the mitochondrial damage-induced kinase PINK1 emerges as a central player. Along with other nuclear encoded mitochondrial proteins, its mRNA associates with mitochondria to sustain mitochondrial function locally. It also regulates mitochondrial degradation, via regulation of proteases, the generation of mitochondria-derived vesicles and mitophagy. In this review, we provide a general overview of the mechanisms governing mitochondrial health in neurons, with a special focus on the role of PINK1 in this endeavor.

## Linked entities

- **Genes:** PINK1 (PTEN induced kinase 1) [NCBI Gene 65018]

## Full-text entities

- **Genes:** PINK1 (PTEN induced kinase 1) [NCBI Gene 65018] {aka BRPK, PARK6}
- **Diseases:** mitochondrial dysfunction (MESH:D028361)

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12858718/full.md

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Source: https://tomesphere.com/paper/PMC12858718