The article discusses the role of cellular senescence in acute kidney injury (AKI), focusing on the senescence of renal tubular epithelial cells (RTECs). Cellular senescence is an irreversible state characterized by cell-cycle arrest, secretion of senescence-associated secretory phenotypes (SASPs), and apoptotic resistance. RTEC senescence is a critical event in the progression of AKI, inhibiting renal regeneration and promoting the transition to chronic kidney disease (CKD). The mechanisms underlying cellular senescence include telomere shortening, DNA damage, mitochondrial dysfunction, metabolic disorders, endoplasmic reticulum stress, and epigenetic regulation. Strategies to inhibit RTEC senescence, target the clearance of senescent RTECs, or promote their apoptosis hold promise for improving the prognosis of AKI. The review highlights the characteristics and mechanisms of RTEC senescence, the impact of intervening RTEC senescence on AKI prognosis, and potential therapeutic approaches.The article discusses the role of cellular senescence in acute kidney injury (AKI), focusing on the senescence of renal tubular epithelial cells (RTECs). Cellular senescence is an irreversible state characterized by cell-cycle arrest, secretion of senescence-associated secretory phenotypes (SASPs), and apoptotic resistance. RTEC senescence is a critical event in the progression of AKI, inhibiting renal regeneration and promoting the transition to chronic kidney disease (CKD). The mechanisms underlying cellular senescence include telomere shortening, DNA damage, mitochondrial dysfunction, metabolic disorders, endoplasmic reticulum stress, and epigenetic regulation. Strategies to inhibit RTEC senescence, target the clearance of senescent RTECs, or promote their apoptosis hold promise for improving the prognosis of AKI. The review highlights the characteristics and mechanisms of RTEC senescence, the impact of intervening RTEC senescence on AKI prognosis, and potential therapeutic approaches.