DC Field | Value | Language |
dc.contributor.author | Pădure, Cătălina | |
dc.contributor.author | Capcelea, Svetlana | |
dc.date.accessioned | 2020-11-09T11:58:28Z | |
dc.date.available | 2020-11-09T11:58:28Z | |
dc.date.issued | 2020-10 | |
dc.identifier.uri | http://repository.usmf.md/handle/20.500.12710/12720 | |
dc.identifier.uri | https://stiinta.usmf.md/ro/manifestari-stiintifice/zilele-universitatii | |
dc.description | Department of Molecular Biology and Human Genetics, State University of Medicine and Pharmacy "Nicolae Testemiteanu" Chișinău, Republic of Moldova, Congresul consacrat aniversării a 75-a de la fondarea Universității de Stat de Medicină și Farmacie „Nicolae Testemițanu” din Republica Moldova, Ziua internațională a științei pentru pace și dezvoltare | en_US |
dc.description.abstract | Introduction: Senescence is the last stage of the physiological development of the human
body, in which the cell division stops and the accumulation of damaged cells
takes place. Trigger factors are DNA damage, telomere shortening, activation
of oncogenic mutations/inactivation of tumor suppressor genes. Purpose: The correlation between the molecular-genetic aspects of senescence and the
exponential increase in the risk of developing malignant tumors with age. Material and methods: Analysis of 25 PubMed scientific articles. Results: Senescence has an impact on aging through 2 mechanisms:
1st With age senescent cells accumulate in tissues, maintaining their status
like this for years, affecting the normal structure and function.
2nd Senescence can limit the regenerative potential of adult stem cells. One explanation is that aged organisms accumulate more genetic, epigenetic
changes than young do. Having shorter telomeres, higher levels of damaged
DNA, aged organisms are more resistant to oncogene proliferation than young
are. Studies have shown that a higher incidence of malignancies in old age
reflects the time required for the accumulation of oncogenic mutations. Besides aging and cancer, the same mechanisms of cellular senescence can
contribute to the development of cardiovascular diseases, atherosclerosis,
type 2 diabetes, osteoarthritis, sarcopenia, neurodegenerative disorders etc. Conclusions: Despite the fact that the genetic program in Homo sapiens provides a
longevity of 140 years, the average age is 72.28 years (according to United
Nations, World Population Prospects 2019). Numerous genetic factors both
inherited and acquired, internal and external environmental factors can
accelerate program depletion, cell senescence, aging of the body and the
development of cancer.
Considering that senescence can have both beneicial and detrimental
effects, pro-senescence and anti-senescence approaches could improve
research into the treatment of the age-related diseases, prevention of many
geriatric problems and improving the general health span of aged individuals. | en_US |
dc.language.iso | en | en_US |
dc.publisher | Universitatea de Stat de Medicină şi Farmacie "Nicolae Testemiţanu" | en_US |
dc.subject | senescence | en_US |
dc.subject | oncogenic mutations | en_US |
dc.subject | DNA | en_US |
dc.subject | aging | en_US |
dc.subject | cancer | en_US |
dc.title | Molecular and genetic aspects of senescence | en_US |
dc.type | Other | en_US |
Appears in Collections: | Culegere de postere
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