Qprt, short for Quinolinate phosphoribosyltransferase, is a rate-limiting enzyme encoding the uronic acid pathway. It is involved in cell cycle progression, cancer cell metabolism, and is a key enzyme in the de novo biosynthesis of nicotinamide adenine dinucleotide (NAD+) from tryptophan [2,3,4,7].

In QPRT-KO mice, the conversion ratio of tryptophan to quinolinic acid was higher than expected, but QPRT was not the rate-limiting enzyme in the conversion of tryptophan to nicotinamide (Nam) [4]. Deletion of Qprt in mice led to decreased ovarian NAD+ levels, accelerating ovarian aging, with subfertility, irregular estrous cycles, and reduced ovarian reserve [6]. In the context of acute kidney injury (AKI), QPRT expression declined in two models of AKI. Haploinsufficient (QPRT+/-) mice had higher quinolinate, lower NAD+, and higher AKI susceptibility [1,7]. In breast cancer, high QPRT expression was associated with a poor prognosis and promoted cancer progression through the PI3K/Akt signaling pathway [2,3,5]. Knockdown of QPRT in human embryonic kidney cells affected cell-cycle progression and proliferation [8].

In conclusion, Qprt is crucial for NAD+ biosynthesis and plays important roles in multiple biological processes and disease conditions. The use of Qprt KO/CKO mouse models has revealed its significance in ovarian aging, AKI, and cancer, helping to understand the underlying mechanisms and potentially providing new targets for treatment.