Nron, also known as long non-coding RNA repressor of the nuclear factor of activated T cells, is a highly conserved long non-coding RNA. It plays diverse roles in multiple biological processes, including glucose/lipid metabolism, energy expenditure, tumorigenesis, and bone-related processes. It is involved in pathways such as PER2/Rev-Erbα/FGF21 axis, MDM2-mediated tumor-suppressing pathways, and NF-κB signaling in osteoclasts [1,2,3].

In diet-induced obesity (DIO) mouse models, Nron knockout (NKO) mice showed metabolic benefits like reduced body weight, fat mass, improved insulin sensitivity, and enhanced adipose function. Nron deletion improved hepatic lipid homeostasis via the PER2/Rev-Erbα/FGF21 axis coupled with AMPK activation [1]. In osteoclast-specific Nron knockout and transgenic mice, Nron effectively inhibited osteoclastogenesis and alveolar bone resorption in periodontitis, and controlled osteoclast maturation during orthodontic bone resorption by regulating NFATc1 nuclear translocation [3,4].

In conclusion, Nron is a key regulator in metabolism, tumorigenesis, and bone-related processes. Gene-knockout mouse models, especially in the context of obesity-related metabolic diseases and bone-resorption-associated conditions like periodontitis and orthodontic bone resorption, have significantly contributed to revealing the biological functions of Nron, providing potential therapeutic targets for these diseases.