Telomeres are repetitive DNA sequences located at the ends of chromosomes. As cells divide, telomeres shorten, ultimately limiting cell replication. Stem cells use the enzyme telomerase to maintain telomere length, but its activity decreases with age, leading to shorter telomeres and more senescent cells. Conversely, cancer cells exploit telomerase to bypass replication limits. The relationship between aging and cancer involves genetic mutations, decreased DNA repair, and chronic inflammation. Understanding telomere biology and inflammation may reveal new approaches for cancer treatment and age-related diseases.
The interconnected complexities of aging, cancer, and inflammation involve genetic mutations, declining DNA repair mechanisms, and increased cancer risk. Chronic inflammation, common in aging and cancer, fosters an environment conducive to cancer development. A comprehensive understanding of molecular and cellular processes is essential for personalized cancer prevention and treatment strategies.
Recent studies highlight the impact of chronic inflammation on immune aging and telomere biology in various health conditions, including cancer. Chronic inflammation accelerates aging, depleting stem cells, disrupting cellular communication, and causing telomere shortening. Telomerase plays a crucial role in maintaining telomere length in highly proliferative cells like hematopoietic progenitors and effector leukocytes. The interaction between inflammation and telomere biology in cancer development underscores the need for identifying new therapeutic targets to manage age-related disorders.
Link: https://doi.org/10.3390/ijms25158542
