MIOX, or myo-inositol oxygenase, is an enzyme that catalyzes the conversion of myo-inositol into glucuronic acid [3]. It is involved in multiple biological processes and associated with various pathways, playing a role in cellular redox balance, energy homeostasis, and lipid peroxidation-related processes [1,4]. Genetic models, such as KO mouse models, are valuable for studying MIOX's functions.

In cisplatin-induced acute kidney injury, MIOX overexpression exacerbates tubular damage by accelerating ferroptosis, as cisplatin-treated MIOX-Tg mice had more severe renal pathological changes and perturbations in ferroptosis metabolic sensors compared to WT mice, while MIOX-KO mice had minimal such changes [1]. In diabetes, MIOX-TG mice showed worsening renal functions with increased oxidant/ER stress and accelerated tubulointerstitial fibrosis, while these changes were not seen in MIOX-KO mice [2]. Also, in obesity-related renal injury, MIOX-TG mice had remarkable derangements in tubular injury biomarkers and decreased expression of p-AMPKα, an effect reversed in ob/MIOXKO mice [4].

In conclusion, MIOX plays a crucial role in processes related to kidney injury, including those associated with ferroptosis, diabetes-induced tubulointerstitial injury, and obesity-related renal injury. The use of MIOX KO/CKO mouse models has been instrumental in revealing these roles, providing insights into the mechanisms underlying these disease conditions and potentially guiding future therapeutic strategies [1,2,4].