MIOX, short for myo-inositol oxygenase, is an enzyme that catalyzes the conversion of myo-inositol into glucuronic acid [4]. It is involved in multiple biological processes and pathways, such as redox regulation, and is of great importance in maintaining cellular homeostasis. Genetic models like KO mouse models have been crucial in studying its functions.

In cisplatin-induced acute kidney injury (AKI), MIOX-overexpressing transgenic (MIOX-Tg) mice had more severe renal pathological changes, increased levels of urea, creatinine, and KIM-1, more tubular injury and apoptosis compared to cisplatin-treated wild-type (WT) mice. In contrast, MIOX-knockout (MIOX-KO) mice had alleviated effects, suggesting that MIOX exacerbates tubular damage in cisplatin-induced AKI [2,5]. In diabetes, MIOX-TG mice had worsening renal functions with increased oxidant/ER stress and accelerated tubulointerstitial fibrosis, while these changes were not seen in MIOX-KO mice, indicating that MIOX expression accentuates tubulointerstitial injury in diabetes [3]. In clear cell renal cell carcinoma (ccRCC), bioinformatics analysis and validation showed that MIOX was down-regulated in tumor epithelial cells, and overexpression of MIOX in ccRCC cells inhibited cell proliferation, migration, invasion, and promoted apoptosis [1].

In conclusion, MIOX plays a significant role in various disease conditions, especially in renal-related diseases like AKI and diabetic renal injury, as well as in cancer progression. The use of MIOX KO mouse models has been instrumental in revealing its function in these disease areas, helping to understand the underlying mechanisms and potentially guiding the development of new therapeutic strategies.