Wsb1, or WD repeat and suppressor of cytokine signaling box containing 1, is a substrate recognition protein within an E3 ubiquitin ligase [1]. It plays roles in diverse biological processes such as thyroid hormone homeostasis, immune regulation, cellular metabolism (including glucose metabolism and hypoxia), and is involved in pathways like β -catenin signaling, NF -κB termination, and more [1,3]. Its dysregulation has been associated with various diseases, especially cancer, highlighting its biological importance [1,2]. Genetic models, like gene knockout (KO) mouse models, can be valuable for studying its functions.

In lung fibrosis, conditional deletion of Wsb1 in adult mice ameliorated bleomycin-induced pulmonary fibrosis, showing that Wsb1 promotes myofibroblast accumulation and attenuates alveolar epithelial regeneration [4]. In myocardial ischemia-reperfusion injury, overexpression of Wsb1 relieved injury-induced cardio dysfunction, while silencing Wsb1 exacerbated cardiomyocyte apoptosis, indicating that Wsb1 restrains myocardial injury by activating β -catenin signaling via promoting GSK3β ubiquitination [5].

In conclusion, Wsb1 is crucial in multiple biological processes and disease conditions. Model-based research, especially KO/CKO mouse models, has revealed its roles in diseases like lung fibrosis and myocardial ischemia-reperfusion injury. Understanding Wsb1 functions helps in grasping the underlying mechanisms of these diseases and may provide potential therapeutic targets.