The article reviews the concept of cellular senescence, a critical feature of mammalian cells that suppresses tumorigenesis. Senescence is characterized by a stable and long-term loss of proliferative capacity, despite continued viability and metabolic activity. The primary cause of replicative senescence is telomere shortening, which triggers a DNA damage response (DDR) and leads to cell cycle arrest. The p53 and p16INK4A-RB pathways are key mediators of this process. Senescence can also be induced by stress, oncogene activation, and loss of tumor suppressors. The article discusses the biomarkers and mechanisms of senescence, including cell cycle arrest, morphological changes, activation of tumor suppressor networks, induction of senescence-associated β-galactosidase (SA-β-GAL) activity, and the formation of senescence-associated heterochromatic foci (SAHF). It highlights the role of reactive oxygen species (ROS) and autophagy in senescence. The article also explores the identification of senescent cells in vitro and in vivo, emphasizing the need for multiple markers to accurately identify senescent cells. Finally, it discusses the pathophysiological implications of senescence, including its role in aging and age-related diseases, as well as its potential benefits in preventing tumorigenesis.The article reviews the concept of cellular senescence, a critical feature of mammalian cells that suppresses tumorigenesis. Senescence is characterized by a stable and long-term loss of proliferative capacity, despite continued viability and metabolic activity. The primary cause of replicative senescence is telomere shortening, which triggers a DNA damage response (DDR) and leads to cell cycle arrest. The p53 and p16INK4A-RB pathways are key mediators of this process. Senescence can also be induced by stress, oncogene activation, and loss of tumor suppressors. The article discusses the biomarkers and mechanisms of senescence, including cell cycle arrest, morphological changes, activation of tumor suppressor networks, induction of senescence-associated β-galactosidase (SA-β-GAL) activity, and the formation of senescence-associated heterochromatic foci (SAHF). It highlights the role of reactive oxygen species (ROS) and autophagy in senescence. The article also explores the identification of senescent cells in vitro and in vivo, emphasizing the need for multiple markers to accurately identify senescent cells. Finally, it discusses the pathophysiological implications of senescence, including its role in aging and age-related diseases, as well as its potential benefits in preventing tumorigenesis.