Mmp10, also known as Stromelysin-2, is a matrix metalloproteinase involved in various immune-related and disease-associated processes. It plays a role in controlling macrophage activation and is associated with pathways such as the PPARγ-STAT3 signaling pathway. MMP10 is crucial for maintaining the balance of immune responses and has overall biological importance in tissue repair, inflammation regulation, and disease development [1,2,9]. Genetic models, especially knockout (KO) mouse models, have been valuable in studying its functions.

In non-alcoholic steatohepatitis (NASH), MMP10-OE mice showed diminished hepatic steatosis and inflammation, while MMP10-KO mice had an imbalanced M1/M2 macrophage ratio and aggravated NASH progression. The PPARγ-MMP10-STAT3 axis promoted M2 macrophage polarization, alleviating NASH [1]. In the tolerance to TLR7-induced skin inflammation, Mmp10-/-mice failed to develop immune hypo-responsiveness, indicating MMP10's role in TLR7-mediated tolerance [2]. In ischemic stroke, the rs17860949 polymorphism in MMP10 was associated with a reduced risk, especially in certain subgroups [3]. In tongue cancer, MMP10 overexpression promoted lymph node metastasis, while its knockdown suppressed it, and miR-944 negatively regulated MMP10 [4]. In a diabetic murine model of ischemic stroke, MMP10 treatment was more effective than tPA in reducing infarct size and neurodegeneration [5]. In tracheal fibrosis, SOX9 promoted ECM deposition through up-regulating MMP10, and SOX9 knockdown ameliorated tracheal fibrosis [6]. In colitis and colon tumorigenesis, miR-148/152 family deficiency elevated MMP10, disrupting the intestinal barrier and activating NF-κB signaling [7]. In steroid-induced osteonecrosis of the femoral head, the rs470154 polymorphism in MMP10 was associated with an increased risk [8]. In acute infection, Mmp10-/-mice had a more severe pro-inflammatory response, and adoptive transfer of wild-type macrophages normalized the morbidity, showing MMP10's role in moderating macrophage-mediated inflammation [9]. In rheumatoid arthritis, miR-496 negatively regulated MMP10, affecting the proliferation and apoptosis of fibroblast-like synoviocytes via the NF-κB signaling pathway [10].

In conclusion, MMP10 plays essential roles in multiple biological processes, especially in macrophage-mediated immune responses, inflammation regulation, and fibrosis. Studies using KO mouse models have revealed its significance in diseases like NASH, ischemic stroke, tongue cancer, colitis, and more, providing potential therapeutic targets for these diseases.