SFXN2 contributes mitochondrial dysfunction-induced apoptosis as a substrate of Parkin.

ABSTRACT:

Introduction

Mitochondria, situated at the center of intricate signaling networks, play crucial roles in maintaining health and driving disease progression. SFXN2, a recently identified member of the mitochondrial transporter family, is localized to the outer mitochondrial membrane and regulates several critical mitochondrial functions, including iron metabolism, heme biosynthesis, bioenergetics, and redox homeostasis. New evidence also suggests a connection between SFXN2 and mitochondrial dysfunction related human diseases such as Parkinson's disease (PD). Despite growing insights into SFXN2's roles across various mitochondrial functions, its regulation under mitochondrial dysfunction and the resulting biological consequences remains unclear.

Methods

The expression levels o

SUBMITTER: Luo S 

PROVIDER: S-EPMC12391048 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature