Mmp15, also known as MT2-MMP, is a member of the membrane-type (MT) MMPs subgroup of matrix metalloproteinases. These zinc-containing endopeptidases can degrade extracellular matrix (ECM) proteins, and Mmp15 is involved in processes like extracellular matrix remodeling and associated signaling cascades, which are crucial for normal development and various physiological functions [1].

In mouse models, Mmp15-deficient mammary glands can still form intact ductal networks, but transcriptome profiling shows that Mmp15 has a key role in regulating mammary gland adipocyte differentiation, specifically controlling the formation of thermogenic brown fat [3]. In cardiac development, Snai1 knockdown in mice leads to decreased Mmp15 expression in endocardial cushions, and Snai1 overexpression promotes Mmp15 expression, cell transformation, and mesenchymal cell migration and invasion. Also, catalytically active MMP15 promotes cell motility in this context [2].

In conclusion, Mmp15 is important for extracellular matrix-related processes. Mouse models have revealed its roles in adipocyte fate determination in the mammary gland and in endocardial cushion development. Understanding Mmp15's functions through these models can provide insights into related physiological and pathological conditions, such as abnormal cardiac valve development and adipose tissue-related disorders [2,3].