Cellular senescence is a critical biological process that plays a significant role in aging and age-related diseases. This article will explore the concept of cellular senescence, its causes, mechanisms, and implications for human health and longevity.
Cellular senescence is a state of permanent cell cycle arrest in which cells cease to divide but remain metabolically active. This process was first described by Leonard Hayflick and Paul Moorhead in 1961, who observed that human fibroblasts had a limited capacity to divide in culture [1].
Several factors can trigger cellular senescence:
As cells divide, their telomeres (protective structures at the ends of chromosomes) shorten. When telomeres reach a critical length, cells enter senescence [2].
Accumulation of DNA damage, whether from external sources (e.g., radiation, chemicals) or internal processes (e.g., oxidative stress), can induce senescence [3].
Activation of certain oncogenes can trigger a senescence response, known as oncogene-induced senescence (OIS), which acts as a tumor suppressor mechanism [4].
Alterations in chromatin structure and gene expression patterns can lead to senescence [5].