Cellular senescence is a process where cells stop dividing and undergo distinct phenotypic changes, including chromatin and secretome alterations, and tumor suppressor activation. Initially viewed as a static endpoint, senescence is now understood as a dynamic, multi-step process involving progressive and diverse cellular states. Senescence plays roles in development, tissue repair, aging, and age-related diseases. It is induced by various stresses, including telomere attrition, DNA damage, and oncogenic signals, and involves pathways like p53-p21 and p16-Ink4a-RB. Senescent cells secrete pro-inflammatory factors, contributing to tissue dysfunction and aging. Senescence can be acute or chronic, with chronic senescence involving long-term cell cycle arrest and persistent senescent cells. Senescent cells in tissues like skeletal muscle, fat, and the eye show elevated markers and premature functional decline. Clearance of senescent cells, as shown in BubR1 progeroid mice, delays age-related pathologies. Senescent cells also contribute to tissue repair and fibrosis control. Senescence in post-mitotic cells, such as neurons, is associated with DNA damage and senescence-like features. Senescent cells accumulate with age and may promote inflammation and tissue deterioration. Targeting senescent cells for clearance is a promising therapeutic strategy for age-related diseases. However, challenges remain in understanding the mechanisms and effects of senescent cell clearance in humans. Future research aims to explore the role of senescent cells in aging, develop targeted therapies, and understand their impact on tissue health and lifespan.Cellular senescence is a process where cells stop dividing and undergo distinct phenotypic changes, including chromatin and secretome alterations, and tumor suppressor activation. Initially viewed as a static endpoint, senescence is now understood as a dynamic, multi-step process involving progressive and diverse cellular states. Senescence plays roles in development, tissue repair, aging, and age-related diseases. It is induced by various stresses, including telomere attrition, DNA damage, and oncogenic signals, and involves pathways like p53-p21 and p16-Ink4a-RB. Senescent cells secrete pro-inflammatory factors, contributing to tissue dysfunction and aging. Senescence can be acute or chronic, with chronic senescence involving long-term cell cycle arrest and persistent senescent cells. Senescent cells in tissues like skeletal muscle, fat, and the eye show elevated markers and premature functional decline. Clearance of senescent cells, as shown in BubR1 progeroid mice, delays age-related pathologies. Senescent cells also contribute to tissue repair and fibrosis control. Senescence in post-mitotic cells, such as neurons, is associated with DNA damage and senescence-like features. Senescent cells accumulate with age and may promote inflammation and tissue deterioration. Targeting senescent cells for clearance is a promising therapeutic strategy for age-related diseases. However, challenges remain in understanding the mechanisms and effects of senescent cell clearance in humans. Future research aims to explore the role of senescent cells in aging, develop targeted therapies, and understand their impact on tissue health and lifespan.