Mgp, also known as Matrix Gla protein, is a vitamin K-dependent, γ-carboxylated protein. Initially identified as a physiological suppressor of ectopic calcification, it also acts as the causal agent of Keutel syndrome. Mgp is involved in various biological processes, including cell differentiation and tumorigenesis, and may participate in pathways such as the NF-κB and BMP2/SMAD pathways [1,3,5,7].

In cancer research, Mgp has been widely studied. In colorectal cancer, Mgp promotes CD8+ T cell exhaustion by activating the NF-κB pathway, leading to liver metastasis. Inhibition of Mgp can decrease the rate of liver metastasis, and combined with αPD1, it can synergistically resist metastasis [1]. Mgp also promotes colon cancer proliferation by enriching intracellular calcium concentration and activating the NF-κB pathway [6]. In breast cancer, MGP+ tumor-associated macrophages facilitate immunoresistance [4]. Additionally, Mgp expression is correlated with disease progression in several cancers, and its methylation status shows differences between healthy and tumoral tissues, suggesting its potential as a prognostic indicator [2]. In perivascular adipose-derived stem cells, Mgp promotes differentiation toward smooth muscle cells via the BMP2/SMAD pathway, enhancing neointimal formation [3].

In conclusion, Mgp plays diverse and significant roles in multiple biological processes and diseases. Its function in promoting cancer progression and affecting the immune microenvironment, as well as its role in vascular remodeling, has been revealed through various studies. The use of models to study Mgp provides insights into these biological functions and potential therapeutic targets for related diseases.