Cellular senescence, a process that permanently arrests cell proliferation in response to various stressors, is increasingly recognized as a key contributor to aging and age-related diseases. While senescence in cultured cells has been extensively studied, understanding senescence in living organisms remains challenging due to technical limitations in identifying and characterizing senescent cells. However, recent evidence suggests that senescence may have beneficial roles, such as directing wound repair and embryogenesis, and that indiscriminate targeting of senescent cells could have negative consequences. The study discusses current progress and challenges in understanding the stressors that induce senescence in vivo, the cell types prone to senescence, and the autocrine and paracrine properties of senescent cells in aging and age-related diseases. Senescence is linked to aging through mechanisms such as the senescence-associated secretory phenotype (SASP), which produces pro-inflammatory and matrix-degrading molecules. Senescent cells may be cleared by immune cells due to SASP factors, which can have tumor-suppressive effects. However, chronic or therapy-induced senescence can be detrimental, leading to tissue dysfunction and disease. Senescence in normal aging, age-related diseases, and therapeutic interventions is a complex process, with senescent cells accumulating in tissues and organs. The study highlights the role of senescence in aging and disease, including its impact on tissue function, stem cell maintenance, and disease progression. Senescence in age-related diseases such as type 2 diabetes and atherosclerosis is influenced by factors such as inflammation, oxidative stress, and telomere attrition. Senescence can drive disease progression by impairing tissue repair and increasing the risk of complications. Therapy-induced senescence, such as that caused by cancer treatments or organ transplants, can lead to premature aging and tissue damage. Targeting senescent cells through senotherapies, such as senolysis or SASP inhibition, is an emerging therapeutic strategy to combat aging and age-related diseases. However, challenges remain in identifying and clearing senescent cells without affecting beneficial senescent cells. The study emphasizes the need for further research to understand the role of senescence in aging and to develop effective therapies for age-related diseases.Cellular senescence, a process that permanently arrests cell proliferation in response to various stressors, is increasingly recognized as a key contributor to aging and age-related diseases. While senescence in cultured cells has been extensively studied, understanding senescence in living organisms remains challenging due to technical limitations in identifying and characterizing senescent cells. However, recent evidence suggests that senescence may have beneficial roles, such as directing wound repair and embryogenesis, and that indiscriminate targeting of senescent cells could have negative consequences. The study discusses current progress and challenges in understanding the stressors that induce senescence in vivo, the cell types prone to senescence, and the autocrine and paracrine properties of senescent cells in aging and age-related diseases. Senescence is linked to aging through mechanisms such as the senescence-associated secretory phenotype (SASP), which produces pro-inflammatory and matrix-degrading molecules. Senescent cells may be cleared by immune cells due to SASP factors, which can have tumor-suppressive effects. However, chronic or therapy-induced senescence can be detrimental, leading to tissue dysfunction and disease. Senescence in normal aging, age-related diseases, and therapeutic interventions is a complex process, with senescent cells accumulating in tissues and organs. The study highlights the role of senescence in aging and disease, including its impact on tissue function, stem cell maintenance, and disease progression. Senescence in age-related diseases such as type 2 diabetes and atherosclerosis is influenced by factors such as inflammation, oxidative stress, and telomere attrition. Senescence can drive disease progression by impairing tissue repair and increasing the risk of complications. Therapy-induced senescence, such as that caused by cancer treatments or organ transplants, can lead to premature aging and tissue damage. Targeting senescent cells through senotherapies, such as senolysis or SASP inhibition, is an emerging therapeutic strategy to combat aging and age-related diseases. However, challenges remain in identifying and clearing senescent cells without affecting beneficial senescent cells. The study emphasizes the need for further research to understand the role of senescence in aging and to develop effective therapies for age-related diseases.