Mmp3, also known as stromelysin-1, is an enzyme belonging to the matrix metalloproteinase family. It plays a crucial role in degrading the extracellular matrix, which is important for normal physiological processes such as tissue remodeling and cell migration. It is also involved in inflammatory pathways, like those related to tumor necrosis factor-alpha (TNF-α) and NF-κB [3].

Mmp3 has been implicated in several diseases. In rheumatoid arthritis (RA), serum levels of MMP3 positively reflect disease activity, joint and bone injury, radiological erosion, and can predict disease outcome and drug responsiveness, suggesting it could be used in personalized medical management of RA [1]. In severe COVID-19, it has been investigated as a diagnostic biomarker and potential therapeutic target [2]. For ankylosing spondylitis (AS), it contributes to both joint destruction and the progression of cardiovascular diseases by degrading the extracellular matrix and destabilizing atherosclerotic plaques, indicating that its inhibition could be a therapeutic strategy to reduce cardiovascular risk in AS patients [3]. In familial Mediterranean fever (FMF), MMP3 levels are significantly higher during attacks compared to healthy controls, which might aid in diagnosing FMF attacks [4]. In the context of cerebral stroke, certain gene polymorphisms of MMP3 are associated with the risk of ischemic and hemorrhagic stroke in the Chinese Han population [5]. In skin-bearing vascularized composite allotransplantation, serum MMP3 protein is a promising marker for stratifying patients according to the severity of rejection [6].

In conclusion, Mmp3 is essential for extracellular matrix degradation and is involved in multiple disease-related processes. Research on Mmp3, especially through genetic models in relevant diseases, provides valuable insights into disease mechanisms and potential therapeutic strategies for conditions like RA, COVID-19, AS, FMF, cerebral stroke, and allotransplant rejection.