Cellular Senescence: Molecular Targets, Biomarkers, and Senolytic Drugs
Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu časopisecké články, přehledy
Grantová podpora
LM2018133
Ministry of School, Education, Youth and Sports of the Czech Republic
CZ.02.1.01/0.0/0.0/16_019/0000868
Ministry of School, Education, Youth and Sports of the Czech Republic
TE02000058
Technological agency of the Czech Republic
IGA_LF_2021_036
Palacky University in Olomouc
PubMed
35456986
PubMed Central
PMC9028163
DOI
10.3390/ijms23084168
PII: ijms23084168
Knihovny.cz E-zdroje
- Klíčová slova
- aging, cellular model, mouse model, senescence, senolytics,
- MeSH
- biologické markery MeSH
- kontrolní body buněčného cyklu MeSH
- poškození DNA MeSH
- stárnutí buněk * genetika MeSH
- stárnutí * genetika MeSH
- zvířata MeSH
- Check Tag
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- biologické markery MeSH
Cellular senescence is defined as irreversible cell cycle arrest caused by various processes that render viable cells non-functional, hampering normal tissue homeostasis. It has many endogenous and exogenous inducers, and is closely connected with age, age-related pathologies, DNA damage, degenerative disorders, tumor suppression and activation, wound healing, and tissue repair. However, the literature is replete with contradictory findings concerning its triggering mechanisms, specific biomarkers, and detection protocols. This may be partly due to the wide range of cellular and in vivo animal or human models of accelerated aging that have been used to study senescence and test senolytic drugs. This review summarizes recent findings concerning senescence, presents some widely used cellular and animal senescence models, and briefly describes the best-known senolytic agents.
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The kinetics of uracil-N-glycosylase distribution inside replication foci