FOXJ2, a member of the Forkhead box transcription factors family, is involved in multiple biological processes. It has been associated with pathways like Notch signaling and is crucial for normal spermatogenesis, cell proliferation, migration, and inflammation regulation [2-6, 9, 10]. Genetic models, such as KO/CKO mouse models, have been instrumental in understanding its functions.

In male mice, FOXJ2 is specifically expressed in meiotic spermatocytes. Using a germ cell-specific conditional knockout model (Foxj2(flox/flox), Mvh-Cre), loss of FOXJ2 led to meiotic arrest and complete infertility, as Foxj2-deficient spermatocytes failed to form chromosomal synapses and perform DSB repair, with reduced expression of related factors [3]. In prostate carcinoma cells, over-expression of FOXJ2 inhibited proliferation, migration, and epithelial-mesenchymal transition through inactivation of the Jagged-1/Notch-1/Hes-1 pathway [2]. In a mouse model of vascular antiphospholipid syndrome (APS), FOXJ2 over-expression, mediated by H3K4me3, accelerated APS pathogenesis by triggering inflammation and thrombosis via the SLAMF8/TREM1 axis [1].

In conclusion, FOXJ2 plays essential roles in spermatogenesis, cancer-related cell behaviors, and inflammatory-thrombotic diseases. Mouse models, especially KO/CKO models, have significantly contributed to understanding its functions in these specific biological processes and disease conditions, providing insights for potential therapeutic strategies in related diseases.