In Vitro’dan In Vivo’ya Yaşlılık Model Teorileri

Year 2024, Volume: 26 Issue: S1, 95 - 99, 30.06.2024

Merve Alpay

https://doi.org/10.18678/dtfd.1500615

Abstract

Bir hücrenin, varsayılan işlevini yerine getiremeyecek kadar yaşlanmasının karşılığı hücrenin biyolojik süreçlerinde her zaman tam bir yetersizliğe yol açmayabilir, hücre yaşlanma mekanizmalarında kademeli bir azalmayı içerir. Hücrenin biyolojik değişimini genetik, yaşam tarzı ve çevresel etkiler gibi faktörler sürdürür. Hücresel yaşlanma kavramı ilk olarak 1961 yılında Hayflick ve çalışma arkadaşları tarafından, in vitro kültüre alınan insan diploid fibroblastlarının çoğalma yetenekleri kalıcı olarak durdurulmadan önce yalnızca sınırlı sayıda hücre bölünmesine maruz kalabileceğini fark ettiklerinde ortaya atıldı. 'Hayflick sınırı' olarak bilinen bu fenomen, daha sonra, birbirini izleyen her hücre bölünmesi turunda telomerlerin kademeli olarak kısalması ile ilişkilendirildi. Yaşlanma süreci boyunca yaşlanan hücreler farklı dokularda toplanmaktadır. Nörodejeneratif ve kardiyovasküler bozukluklar, kanser, böbrekle ilgili değişiklikler, kronik akciğer hastalıkları ve osteoartrit gibi yaşa bağlı sağlık sorunlarına katılımları, yaşlanan hücreleri terapötik olarak hedeflemenin çeşitli sağlık koşullarında umut verici olabileceğini düşündürmektedir. Bu derlemede biyolojik yaşlanmaya bağlı olarak hangi hücre tiplerinin yaşlanabileceğine ve bu süreçlerin yaşla ilişkili dokuya özgü patolojileri nasıl etkileyebileceğine dair mevcut veriler tartışılacaktır. Ek olarak, yaşlanan hücrelerin in vitro ortamdan in vivo ortama fizyolojik geçişini karakterize etmek için kullanılan belirteçler de değerlendirilecektir. Tartışılan veriler, farklı organlarda yaşlanan hücrelerin moleküler ve fonksiyonel özelliklerinin genişletilmiş bir tanımı için önemli bir başlangıç noktası olarak hizmet edebilir, böylece in vivo hedefleme stratejilerinin geliştirilmesini ve artırılmasını destekleyebilir.

Keywords

Hücre yaşlanması, geriatrik in vivo modeller, hücresel yaşlanma teorileri, biyolojik yaşlanma mekanizması

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.

Keywords

Cell senescence, geriatric in vivo models, cellular aging theories, biological aging mechanism

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