Senescence Model Theories from In Vitro through In Vivo

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dc.authorscopusid56078893600en_US
dc.contributor.authorAlpay, M.
dc.date.accessioned2024-08-23T16:07:30Z
dc.date.available2024-08-23T16:07:30Z
dc.date.issued2024en_US
dc.departmentDüzce Üniversitesien_US
dc.description.abstractThe theoretical equivalence of expressing that a cell is aging to its inability to perform the assumed function is not exactly accurate, it involves a gradual decrease in cell aging mechanisms. Factors such as genetics, lifestyle, and environmental effects maintain the biological change of the cell. The concept of cellular senescence was initially introduced by Hayflick and his collaborators in 1961 when they noticed that human diploid fibroblasts cultured in vitro could undergo only a limited number of cell divisions before their ability to proliferate was permanently halted. This phenomenon, known as the 'Hayflick limit', was subsequently linked to the gradual shortening of telomeres with each successive round of cell division. Throughout the aging process, senescent cells collect in different tissues. Their involvement in age-related health issues such as neurodegenerative disorders, heart problems, cancer, kidney-related changes, chronic lung diseases, and osteoarthritis suggests that targeting senescent cells therapeutically could be promising across various health conditions. This review will discuss the available data on which cell types may undergo aging based on biological aging and how these processes may impact age-associated tissue-specific pathologies. Additionally, the markers used to characterize the physiological transition of aging cells from in vitro to in vivo settings will be evaluated. The discussed data may serve as a significant starting point for an expanded definition of the molecular and functional characteristics of aging cells in different organs, thus supporting the development and enhancement of targeting strategies in vivo. © 2024, Duzce University Medical School. All rights reserved.en_US
dc.identifier.doi10.18678/dtfd.1500615
dc.identifier.endpage99en_US
dc.identifier.issn1307-671X
dc.identifier.issueS1en_US
dc.identifier.scopus2-s2.0-85197521190en_US
dc.identifier.scopusqualityQ4en_US
dc.identifier.startpage95en_US
dc.identifier.urihttps://doi.org/10.18678/dtfd.1500615
dc.identifier.urihttps://hdl.handle.net/20.500.12684/14690
dc.identifier.volume26en_US
dc.indekslendigikaynakScopusen_US
dc.institutionauthorAlpay, M.en_US
dc.language.isoenen_US
dc.publisherDuzce University Medical Schoolen_US
dc.relation.ispartofDuzce Medical Journalen_US
dc.relation.publicationcategoryDiğeren_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectbiological aging mechanismen_US
dc.subjectCell senescenceen_US
dc.subjectcellular aging theoriesen_US
dc.subjectgeriatric in vivo modelsen_US
dc.subjectagingen_US
dc.subjectcell agingen_US
dc.subjectcell divisionen_US
dc.subjectchronic lung diseaseen_US
dc.subjectdiploidyen_US
dc.subjectdrug therapyen_US
dc.subjectfibroblasten_US
dc.subjecthumanen_US
dc.subjecthuman cellen_US
dc.subjectin vitro studyen_US
dc.subjectkidney canceren_US
dc.subjectnonhumanen_US
dc.subjectosteoarthritisen_US
dc.subjectpharmacologyen_US
dc.subjectreviewen_US
dc.subjectsenescenceen_US
dc.subjecttelomereen_US
dc.titleSenescence Model Theories from In Vitro through In Vivoen_US
dc.title.alternativeIn Vitro’dan In Vivo’ya Yaşlılık Model Teorilerien_US
dc.typeReviewen_US

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