Senescence Model Theories from In Vitro through In Vivo

Abstract

The 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.