Cell senescence is a state of irreversible cell cycle arrest and simultaneously secretes inflammatory factors, chemokines and other senescence-associated secretory phenotype (SASP), which plays an important role in the progression of kidney diseases, metabolic diseases and other diseases. Renal tubular cell (RTC) senescence is a key cellular biological event in the progression of acute kidney injury (AKI). Senescent RTCs not only inhibit the regeneration and repair of AKI, but also release SASP to promote the progression of AKI. Inhibition of RTC senescence, targeted removal of senescent RTCs or promotion of senescent RTCs apoptosis could improve the prognosis of AKI, indicating that these methods have broad application prospects.
The incidence of acute kidney injury (AKI) has increased rapidly in recent years. The causes of AKI are complex and diverse, and there is no effective treatment strategy. Reliable and stable animal models and in vitro models play an important role in the development and prevention of AKI. Focusing on rodent models and in vitro models, this review summarizes AKI models induced by ischemia, nephrotoxic drugs and urinary tract obstruction from three levels of prerenal, intrinsic renal and postrenal AKI.