Cellular senescence as a key contributor to secondary neurodegeneration in traumatic brain injury and stroke.
Autor: | Huang Z; Department of Neurology, Medical College of Georgia, Augusta University, 1120 15th Street, Augusta, GA, 30912, USA.; Department of Pharmacology, Toxicology and Neuroscience, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, LA, 71103, USA., Xu P; Department of Drug Discovery and Biomedical Sciences, College of Pharmacy, University of South Carolina, 715 Sumter, Columbia, SC, 29208, USA., Hess DC; Department of Neurology, Medical College of Georgia, Augusta University, 1120 15th Street, Augusta, GA, 30912, USA., Zhang Q; Department of Neurology, Medical College of Georgia, Augusta University, 1120 15th Street, Augusta, GA, 30912, USA. qzhang@augusta.edu. |
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Jazyk: | angličtina |
Zdroj: | Translational neurodegeneration [Transl Neurodegener] 2024 Dec 12; Vol. 13 (1), pp. 61. Date of Electronic Publication: 2024 Dec 12. |
DOI: | 10.1186/s40035-024-00457-2 |
Abstrakt: | Traumatic brain injury (TBI) and stroke pose major health challenges, impacting millions of individuals globally. Once considered solely acute events, these neurological conditions are now recognized as enduring pathological processes with long-term consequences, including an increased susceptibility to neurodegeneration. However, effective strategies to counteract their devastating consequences are still lacking. Cellular senescence, marked by irreversible cell-cycle arrest, is emerging as a crucial factor in various neurodegenerative diseases. Recent research further reveals that cellular senescence may be a potential driver for secondary neurodegeneration following brain injury. Herein, we synthesize emerging evidence that TBI and stroke drive the accumulation of senescent cells in the brain. The rationale for targeting senescent cells as a therapeutic approach to combat neurodegeneration following TBI/stroke is outlined. From a translational perspective, we emphasize current knowledge and future directions of senolytic therapy for these neurological conditions. Competing Interests: Declarations. Ethics approval and consent to participate: Not applicable. Consent for publication: All authors have read and approved the final manuscript for publication. Competing interests: The authors declare that they have no competing interests. (© 2024. The Author(s).) |
Databáze: | MEDLINE |
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