Bdkrb2, encoding the bradykinin B2 receptor, plays a crucial role in regulating nitric oxide production, which is involved in controlling vasodilatation [3]. It is also associated with multiple biological processes and disease-related pathways, such as the epithelial-to-mesenchymal transition (EMT) in glioma [2], and is potentially related to the exercise pressor reflex [4]. Genetic models are valuable for studying its functions.

In mouse models, Bdkrb2-/-embryos exposed to gestational salt stress develop renal dysgenesis. The underlying mechanism involves p53 stabilization, apoptosis, and repression of terminal epithelial differentiation. There is also a functional cross-talk between p53 and BdkrB2, where BdkrB2 is a target for p53-mediated transcriptional activation, and BdkrB2 inactivation upregulates Chk1 levels, potentiating p53 phosphorylation on Ser23 by Chk1, leading to renal dysgenesis [1].

In conclusion, Bdkrb2 is essential for vasodilatation regulation and is involved in complex biological processes like those in kidney development and glioma progression. The gene knockout mouse models have significantly contributed to understanding its role in renal dysgenesis, highlighting its importance in related disease areas.