Socs3, a member of the suppressors of cytokine signaling (SOCS) family, is an inducible negative feedback inhibitor of cytokine signaling. It plays a crucial role in regulating cytokine or hormone signaling, mainly by binding to JAK kinase and cytokine receptors, inhibiting STAT3 activation, and also controls other STAT-related and non-STAT-related cellular pathways [3]. It is involved in key pathways such as JAK-STAT signaling and is important for immune homeostasis, energy metabolism, and cell growth regulation [1,2,3]. Conditional deletion of Socs3 in mice using the Cre-lox system has been vital for understanding its functions in different physiological and disease contexts [7].

In mice, Socs3 deficiency in myeloid cells leads to more severe dextran sulfate sodium (DSS)-induced colitis, with increased infiltration of monocytes and neutrophils, indicating its role in preventing over-activation of the immune system in Inflammatory Bowel Diseases [4]. The cardiac-specific deletion of Socs3 enhances cardioprotective signaling pathways, inhibits myocardial apoptosis and fibrosis, and suppresses left ventricular remodeling after myocardial infarction, suggesting it as a potential therapeutic target for cardioprotection [5]. Also, in Mycobacterium tuberculosis infection models, Socs3 is crucial in restraining inflammation and enabling optimal protective immune responses [6].

In conclusion, Socs3 is essential for regulating cytokine signaling, immune responses, and energy metabolism. Mouse models with Socs3 gene knockout or conditional knockout have revealed its significant roles in diseases such as colitis, heart diseases, and tuberculosis infection. These findings provide valuable insights into potential therapeutic strategies targeting Socs3 for treating related diseases.