title: [Impact of cellular senescence on organismal aging and age-related diseases].
abstract: Development of the civilization and medicine enables an even longer lifespan of people. To modulate the aging process it is necessary to discover its molecular mechanism and its causes. It has been known for almost 60 years that cells undergo senescence. A lot of markers of senescence have been described to distinguish senescent cells. Every year we can observe an increase in the number of data, supporting the thesis that the reason for aging of the whole organism is cellular senescence. We age because cells building tissues and organs undergo senescence. It is also believed that cellular senescence can increase the frequency of age-related diseases. The role of cellular senescence strictly depends on the age of the individual. In young ones it is essential for: protection against cancer and tissue regeneration. In old ones it causes tissues and organs dysfunctions and leads to age-related diseases. Slowing down aging could prevent age-related diseases and this seems to be more promising than curing them. To enrich our knowledge concerning aging it is important to understand signaling pathways leading to senescence. Recently a new role of cellular senescence has been discovered, namely during embryogenesis. This observation is very surprising and shows a new face of cellular senescence. It is possible that, similarly to the previously described role of apoptosis in embryogenesis, senescence is indispensable for proper organogenesis. Cellular senescence seems to be the universal and fundamental process, the role of which changes during the lifespan.
authors.forename: Anna
authors.initials: A
authors.lastname: Bielak-Zmijewska
authors.forename: Wioleta
authors.initials: W
authors.lastname: Grabowska
authors.forename: Dorota
authors.initials: D
authors.lastname: Przybylska
mesh_terms: D000375:Aging / Q000473:pathology / Q000502:physiology*; D000818:Animals; D017209:Apoptosis; D016922:Cellular Senescence / Q000502:physiology*; D002908:Chronic Disease; D047108:Embryonic Development / Q000502:physiology; D006801:Humans; D009369:Neoplasms / Q000378:metabolism / Q000473:pathology; D038081:Organogenesis / Q000502:physiology; D018384:Oxidative Stress; D015398:Signal Transduction