Ctss, short for cathepsin S, is a member of the lysosomal cysteine cathepsin family of proteases. It is involved in degrading unwanted and damaged proteins within the lysosome and also mediates roles like antigen processing and presentation, and cleavage of substrates both intra and extracellularly. It has a normal restricted expression profile, inducible upregulation, and activity at a broad pH range, making it a key player in various biological processes [1].

In the context of disease, several studies with mouse models have been revealing. In a mouse FeCl3 model, CTSS-deficient mice (CTSS-/-) showed reduced stress-related thrombosis, with decreased levels of inflammatory and apoptosis-related factors compared to wild-type mice (CTSS + / + ) [2]. In a liver fibrosis study, myeloid-specific Piezo1 knockout mice, which had inhibited expression and activity of CTSS, attenuated liver fibrosis [3]. Also, in a melanoma study, BCG hydrogel promoted CTSS-mediated antigen processing and presentation, suppressing metastasis and prolonging survival in mouse models [4].

In conclusion, Ctss is a multifunctional protease involved in important biological processes such as protein degradation and antigen processing. Mouse models, especially KO models, have been instrumental in uncovering its role in diseases like thrombosis, liver fibrosis, and melanoma, providing insights into potential therapeutic targets for these conditions.