Abstract

UNLOCKING THE SECRETS OF TELOMERE AGING: KEY INSIGHTS INTO CELLULAR LONGEVITY

Dr. D. Nirmala*, Gopagoni Akshitha, Gunnam Laxmi Rushita, Gonepally Rakshitha, Gummidi Jahnavi Sai Sreya and Jatavath Swarnalatha

ABSTRACT

Because telomeres alter how cells respond to stress and growth stimulation depending on DNA damage and previous cell divisions, they are crucial for determining cell fate and aging. Specialized structures known as telomeres are found at the end of linear chromosomes. Together with a protein complex called shelterin, the hexanucleotide sequence TTAGGG is repeated. When together, they provide scaffolding that guards against chromosome fusion and breakage. A DNA damage response that results in senescence or apoptosis is triggered by the uncapped state brought on by telomere shortening or damage and loop opening. The average telomere length, usually measured in human blood lymphocytes, was thought to be a biomarker for aging, survival, and mortality. However, it becomes obvious that regulation of telomere length is very complex and involves multiple processes. For example, the ―end replicationproblem‖ during DNA replication, as well as oxidative stress, are responsible for the shortening of telomeres. In contrast, telomerase activity can potentially counteract telomere shortening when it is able to access and interact with telomeres. However, while highly active during development and in cancer cells, the enzyme is down-regulated in most human somatic cells with a few exceptions, such as human lymphocytes.

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