# FGF–FGFR Signaling in Parkinson’s Disease: Mechanistic Links to Ferroptosis and Neuroprotection

## TL;DR

This paper reviews how FGF–FGFR signaling may protect brain cells in Parkinson’s disease by influencing processes like inflammation and cell death.

## Contribution

The paper highlights novel mechanistic links between FGF–FGFR signaling and ferroptosis in Parkinson’s disease.

## Key findings

- FGF–FGFR signaling modulates mitochondrial quality control and lipid peroxidation.
- FGF signaling intersects with redox homeostasis and iron metabolism, influencing ferroptosis.
- Targeting FGF pathways shows potential as a therapeutic strategy for Parkinson’s disease.

## Abstract

Parkinson’s disease (PD) is characterized by progressive degeneration of the nigrostriatal dopaminergic system and α-synuclein (α-syn) pathology, with disease progression driven by convergent mechanisms including neuroinflammation, mitochondrial injury, oxidative stress, and regulated cell-death programs such as ferroptosis. Fibroblast growth factors (FGFs) and fibroblast growth factor receptors (FGFRs) constitute a key signaling system in the central nervous system, influencing not only neuronal survival and glial states but also intersecting with networks governing redox homeostasis and iron metabolism. Accumulating evidence indicates that, beyond classical neurotrophic actions, FGF–FGFR signaling can modulate mitochondrial quality control, glial inflammatory activation, and lipid peroxidation-related processes, thereby reshaping cellular susceptibility to ferroptotic injury. This review summarizes current advances in understanding FGF signaling networks in Parkinson’s disease, synthesizes their potential mechanistic links to the interplay among neuroinflammation, mitochondrial dysfunction, and redox imbalance as well as to ferroptosis regulation, and discusses the experimental basis and translational challenges of targeting the FGF pathway as a disease-modifying therapeutic strategy.