Unraveling the AKT/ERK cascade and its role in Parkinson disease.
Autor: | Keshri PK; Department of Biochemistry, Institute of Science, Banaras Hindu University, Varanasi, 221005, Uttar Pradesh, India., Singh SP; Department of Biochemistry, Institute of Science, Banaras Hindu University, Varanasi, 221005, Uttar Pradesh, India. sps.biochem23@gmail.com. |
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Jazyk: | angličtina |
Zdroj: | Archives of toxicology [Arch Toxicol] 2024 Oct; Vol. 98 (10), pp. 3169-3190. Date of Electronic Publication: 2024 Aug 13. |
DOI: | 10.1007/s00204-024-03829-9 |
Abstrakt: | Parkinson disease represents a significant and growing burden on global healthcare systems, necessitating a deeper understanding of their underlying molecular mechanisms for the development of effective treatments. The AKT and ERK pathways play crucial roles in the disease, influencing multiple cellular pathways that support neuronal survival. Researchers have made notable progress in uncovering how these pathways are controlled by upstream kinases and how their downstream effects contribute to cell signalling. However, as we delve deeper into their intricacies, we encounter increasing complexity, compounded by the convergence of multiple signalling pathways. Many of their targets overlap with those of other kinases, and they not only affect specific substrates but also influence entire signalling networks. This review explores the intricate interplay of the AKT/ERK pathways with several other signalling cascades, including oxidative stress, endoplasmic reticulum stress, calcium homeostasis, inflammation, and autophagy, in the context of Parkinson disease. We discuss how dysregulation of these pathways contributes to disease progression and neuronal dysfunction, highlighting potential therapeutic targets for intervention. By elucidating the complex network of interactions between the AKT/ERK pathways and other signalling cascades, this review aims to provide insights into the pathogenesis of Parkinson disease and describe the development of novel therapeutic strategies. (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.) |
Databáze: | MEDLINE |
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