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The role of cellular senescence in neurodegenerative diseases
Y. Wang, K. Kuca, L. You, E. Nepovimova, Z. Heger, M. Valko, V. Adam, Q. Wu, K. Jomova
Jazyk angličtina Země Německo
Typ dokumentu časopisecké články, přehledy
Grantová podpora
GA23-05857S
Grantová Agentura České Republiky
University of Granada
Universidad de Granada
Scientific Grant Agency (VEGA Project 1/0542/24)
Universidad de Granada
32373073
National Natural Science Foundation of China
MH CZ - DRO (UHHK
Ministerstvo Zdravotnictví Ceské Republiky
00179906)
Ministerstvo Zdravotnictví Ceské Republiky
VEGA Project 1/0542/24)
Scientific Grant Agency
- MeSH
- Alzheimerova nemoc MeSH
- amyloidní beta-protein metabolismus MeSH
- lidé MeSH
- neurodegenerativní nemoci * MeSH
- Parkinsonova nemoc metabolismus MeSH
- sekreční fenotyp asociovaný se senescencí MeSH
- signální transdukce MeSH
- stárnutí buněk * účinky léků MeSH
- zkracování telomer účinky léků MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
Increasing evidence has revealed that cellular senescence drives NDs, including Alzheimer's disease (AD) and Parkinson's disease. Different senescent cell populations secrete senescence-associated secretory phenotypes (SASP), including matrix metalloproteinase-3, interleukin (IL)-1α, IL-6, and IL-8, which can harm adjacent microglia. Moreover, these cells possess high expression levels of senescence hallmarks (p16 and p21) and elevated senescence-associated β-galactosidase activity in in vitro and in vivo ND models. These senescence phenotypes contribute to the deposition of β-amyloid and tau-protein tangles. Selective clearance of senescent cells and SASP regulation by inhibiting p38/mitogen-activated protein kinase and nuclear factor kappa B signaling attenuate β-amyloid load and prevent tau-protein tangle deposition, thereby improving cognitive performance in AD mouse models. In addition, telomere shortening, a cellular senescence biomarker, is associated with increased ND risks. Telomere dysfunction causes cellular senescence, stimulating IL-6, tumor necrosis factor-α, and IL-1β secretions. The forced expression of telomerase activators prevents cellular senescence, yielding considerable neuroprotective effects. This review elucidates the mechanism of cellular senescence in ND pathogenesis, suggesting strategies to eliminate or restore senescent cells to a normal phenotype for treating such diseases.
Biomedical Research Center University Hospital Hradec Kralove 500 05 Hradec Kralove Czech Republic
College of Life Science Yangtze University Jingzhou 434025 China
Department of Chemistry and Biochemistry Mendel University in Brno 613 00 Brno Czech Republic
Faculty of Chemical and Food Technology Slovak University of Technology 812 37 Bratislava Slovakia
Citace poskytuje Crossref.org
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