Crim1, also known as Cysteine-rich motor neuron1 protein, is a transmembrane protein. It is crucial in regulating growth factor localization, availability, and activity during embryogenesis. Crim1 interacts with growth factors like TGFβs, BMPs, VEGFs, and PDFGs, and is involved in pathways related to organogenesis, angiogenesis, and the epithelial - mesenchymal transition (EMT) [1,2]. It is of great biological importance as it participates in the development of multiple organs including the heart, eye, kidney, and placenta [1]. Genetic models, such as knockout mouse models, have been instrumental in studying its function.

In knockout mouse models, loss of Crim1 leads to congenital heart defects, including epicardial defects and hypoplastic ventricular compact myocardium. Epicardium - restricted deletion of Crim1 increases epithelial - to - mesenchymal transition and invasion of the myocardium in vivo, along with enhanced migration of primary epicardial cells. It is also necessary for the proliferation of epicardium - derived cells and their differentiation into cardiac fibroblasts, as well as normal levels of cardiomyocyte proliferation and apoptosis [3]. In Crim1KST264 mutant mice, loss of Crim1 function in ocular tissues results in inappropriate differentiation of the lens epithelium into fiber cells [4].

In conclusion, Crim1 plays essential roles in organogenesis, especially in heart and eye development. The use of KO mouse models has revealed its cell - autonomous and paracrine roles in heart development, as well as its requirement for maintaining the ocular lens epithelium. Understanding Crim1's functions may provide insights into congenital heart diseases and eye development - related disorders.