ADAM15, a disintegrin and metalloproteinase 15, is a transmembrane protein involved in multiple biological processes such as protein ectodomain shedding, cell adhesion, and signaling [2]. It can interact with molecules intra-and extra-cellularly to mediate various cellular functions [3]. ADAM15 may also be involved in pathways related to cell-cell and cell-extracellular matrix interactions, as well as signal transduction pathways [5,6].

In disease-related research, gene knockout models have provided insights. In Adam15-/-mice after myocardial infarction, there was a higher rate of left ventricular rupture, worsened left ventricular dysfunction, and reduced fibrillar collagen density, indicating ADAM15's role in optimal collagen cross-linking and scar formation [3]. In female Adam15-/-mice with cardiac pressure overload, different responses were observed compared to wild-type mice, suggesting ADAM15 may have a less prominent role in female cardiac response to post-transverse aortic constriction (TAC) remodeling [4]. Also, in male Adam15-/-mice with TAC, there was exacerbated transition to decompensated myocardial hypertrophy and dilation through activation of the calcineurin pathway [7]. In the context of cancer, knockdown of ADAM15 in hepatocellular carcinoma cells promoted apoptosis and suppressed proliferation, migration, and invasion [1]. In colorectal tumors, loss of cancer cell-derived ADAM15 altered the tumor microenvironment, leading to higher immune cell infiltration and cancer cell apoptosis [6].

In conclusion, ADAM15 is crucial for multiple biological functions including cell adhesion, extracellular matrix regulation, and signal transduction. Gene knockout mouse models have revealed its significance in diseases such as heart diseases (myocardial infarction, cardiomyopathies) and cancers (hepatocellular carcinoma, colorectal cancer). Understanding ADAM15's role through these models can potentially offer new therapeutic targets for these diseases.