Abstract
Calcium oxalate (CaOx) stones account for 90% of uroliths in cats and contribute to ureteral inflammation and fibrosis, although the underlying mechanism remains unclear. Apoptosis inhibitor of macrophage (AIM) is known to play a protective role against tubular injury in feline kidney disease. This study investigated whether AIM contributes to ureteral fibrosis by using AIM-felinized mice subjected to CaOx bead-induced ureteral injury. Male C57BL/6 mice (n = 54), including wild-type mice (mA), AIM-knockout (koA) mice, and AIM-felinized mice (fA), were assigned to either a unilateral ureteral obstruction (UUO; U) group or a UUO plus CaOx implantation (C) group. Ureters were collected 14 days after the procedure for histopathological analysis. The severity of ureteral injury followed the order of koA-C ≥ fA-C > mA-C, indicating AIM's involvement in the injury process. Furthermore, fA exhibited more severe fibrosis than mA mice (p < 0.05), suggesting that mouse AIM may have stronger anti-fibrotic effects than feline AIM. These results suggest that AIM-felinized mice could serve as a useful model for investigating feline-specific ureteral pathology. To our knowledge, this is the first experimental study to explore the role of feline AIM in ureteral injury and fibrosis. Further studies are warranted to validate the utility of this model.