Cellular Senescence And Aging: Mechanisms, Disease Convergence, And Therapeutic Frontiers
Our bodies are made of cells, and sometimes these cells enter a state called “cellular senescence.” This means they stop dividing permanently, often due to stress like DNA damage or shortened protective caps on chromosomes called telomeres. While acutely, these “senescent cells” can be helpful, for example, in preventing cancer or aiding wound healing, their chronic accumulation as we age becomes problematic. These cells don’t just sit there; they release a mix of inflammatory molecules, known as the senescence-associated secretory phenotype (SASP), which can spread damage to neighboring cells and contribute to chronic inflammation throughout the body. This sustained inflammation and tissue dysfunction are major drivers of many age-related diseases, including heart disease, neurodegenerative disorders, and metabolic conditions. Understanding how these cells contribute to aging and disease opens up exciting new avenues for treatment. Researchers are exploring therapies like “senolytics,” which are compounds designed to selectively eliminate senescent cells, and “senomorphics,” which aim to change the harmful signals these cells send out. The ultimate goal of these strategies is to extend the period of life spent in good health, known as healthspan.
Source: link to paper