Cellular senescence is an irreversible cell-cycle arrest with senescence-associated secretory phenotype (SASP) and apoptotic resistance. It plays a critical role in embryonic development, tissue regeneration, tumor suppression, and the pathogenesis of age-related diseases, including kidney diseases. In acute kidney injury (AKI), senescence of renal tubular epithelial cells (RTECs) is a key event that impairs renal regeneration and promotes progression to chronic kidney disease (CKD). Mechanisms of RTEC senescence include telomere shortening, DNA damage, mitochondrial dysfunction, endoplasmic reticulum stress, and epigenetic regulation. Strategies to inhibit RTEC senescence, target senescent cell clearance, or promote apoptosis may improve AKI prognosis. RTEC senescence is associated with SASP, which includes inflammatory factors and chemokines that accelerate CKD progression. The role of RTEC senescence in AKI varies depending on stressors, and further research is needed to improve targeting and effectiveness of interventions. Cellular senescence is involved in various physiological and pathological processes, including embryonic development, tissue repair, tumor suppression, and disease progression. It is also linked to neurodegenerative diseases, cancer, diabetes, and kidney diseases. Mechanisms of cellular senescence include DNA damage, telomere shortening, mitochondrial dysfunction, and epigenetic regulation. Targeting senescence through interventions such as calorie restriction, exercise, and drugs like metformin, rapamycin, and resveratrol may improve AKI outcomes. Targeted clearance of senescent cells, such as using p16-positive markers, can alleviate kidney damage and enhance renal function. However, targeting p16-positive cells may cause structural damage and renal dysfunction. Overall, understanding the mechanisms of RTEC senescence in AKI is crucial for developing effective treatments.Cellular senescence is an irreversible cell-cycle arrest with senescence-associated secretory phenotype (SASP) and apoptotic resistance. It plays a critical role in embryonic development, tissue regeneration, tumor suppression, and the pathogenesis of age-related diseases, including kidney diseases. In acute kidney injury (AKI), senescence of renal tubular epithelial cells (RTECs) is a key event that impairs renal regeneration and promotes progression to chronic kidney disease (CKD). Mechanisms of RTEC senescence include telomere shortening, DNA damage, mitochondrial dysfunction, endoplasmic reticulum stress, and epigenetic regulation. Strategies to inhibit RTEC senescence, target senescent cell clearance, or promote apoptosis may improve AKI prognosis. RTEC senescence is associated with SASP, which includes inflammatory factors and chemokines that accelerate CKD progression. The role of RTEC senescence in AKI varies depending on stressors, and further research is needed to improve targeting and effectiveness of interventions. Cellular senescence is involved in various physiological and pathological processes, including embryonic development, tissue repair, tumor suppression, and disease progression. It is also linked to neurodegenerative diseases, cancer, diabetes, and kidney diseases. Mechanisms of cellular senescence include DNA damage, telomere shortening, mitochondrial dysfunction, and epigenetic regulation. Targeting senescence through interventions such as calorie restriction, exercise, and drugs like metformin, rapamycin, and resveratrol may improve AKI outcomes. Targeted clearance of senescent cells, such as using p16-positive markers, can alleviate kidney damage and enhance renal function. However, targeting p16-positive cells may cause structural damage and renal dysfunction. Overall, understanding the mechanisms of RTEC senescence in AKI is crucial for developing effective treatments.