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Physical Exercise-Induced Activation of NRF2 and BDNF as a Promising Strategy for Ferroptosis Regulation in Parkinson’s Disease

Lookup NU author(s): Professor Tiago OuteiroORCiD

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Abstract

© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra. Ferroptosis, an iron-dependent form of regulated cell death, may contribute to the progression of PD owing to an unbalanced brain redox status. Physical exercise is a complementary therapy that can modulate ferroptosis in PD by regulating the redox system through the activation of nuclear factor (erythroid-derived 2)-like 2 (NRF2) and brain-derived neurotrophic factor (BDNF) signaling. However, the precise effects of physical exercise on ferroptosis in PD remain unclear. In this review, we explored how physical exercise influences NRF2 and BDNF signaling and affects ferroptosis in PD. We further investigated relevant publications over the past two decades by searching the PubMed, Web of Science, and Google Scholar databases using keywords related to physical exercise, PD, ferroptosis, and neurotrophic factor antioxidant signaling. This review provides insights into current research gaps and demonstrates the necessity for future research to elucidate the specific mechanisms by which exercise regulates ferroptosis in PD, including the assessment of different exercise protocols and their long-term effects. Ultimately, exploring these aspects may lead to the development of improved exercise interventions for the better management of patients with PD.


Publication metadata

Author(s): Thirupathi A, Marqueze LF, Outeiro TF, Radak Z, Pinho RA

Publication type: Review

Publication status: Published

Journal: Neurochemical Research

Year: 2024

Volume: 49

Pages: 1643-1654

Print publication date: 01/07/2024

Online publication date: 24/05/2024

Acceptance date: 10/05/2024

ISSN (print): 0364-3190

ISSN (electronic): 1573-6903

Publisher: Springer

URL: https://doi.org/10.1007/s11064-024-04152-6

DOI: 10.1007/s11064-024-04152-6


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