Lilrb4a, also known as Leukocyte immunoglobulin-like receptor B4a, is an immunosuppressive regulatory receptor. It is involved in multiple biological processes and associated with various signaling pathways such as NF-κB and MAPK signaling, and is of great importance in cardiovascular, bone, and cancer-related biological systems [1,2,3]. Genetic mouse models are valuable tools for studying its functions.

In the ISO-induced mouse model, Lilrb4a knockout and overexpression mice were used to study its role in cardiac function. The results showed that Lilrb4a alleviated cardiac structural and electrical remodeling and protected against ventricular arrhythmias induced by ISO. The mechanism was that Lilrb4a inhibited NF-κB and MAPK signaling activation mediated by transforming growth factor kinase 1 [1].

In the study of bone turnover in mice expressing constitutively active TGF-β receptor type I, silencing Lilrb4 increased the number of osteoclasts and osteoclast marker genes, indicating its role in osteoclast-related bone regulation [2].

In a study on circadian rhythm disruption (CRD)-induced breast cancer, CRD enhanced Lilrb4a expression, leading to an immunosuppressive tumor microenvironment, and targeted immunotherapy against LILRB4 reduced CRD-induced immunosuppression and lung metastasis [3].

In conclusion, Lilrb4a plays essential roles in cardiovascular function, bone turnover, and tumor-related immunosuppression as revealed through mouse model-based research. The use of Lilrb4a knockout or overexpression mouse models has significantly contributed to understanding its functions in these disease-related areas, providing insights into potential therapeutic targets for cardiac, bone, and cancer-related diseases.