Tnc-flox Mouse

Tenascin-C (Tnc), a large multimodular glycoprotein of the extracellular matrix, has diverse functions. It is involved in processes like cell proliferation, apoptosis, and adhesion, and plays a role in multiple biological pathways. Tnc is highly expressed under pathological conditions and is crucial for understanding various disease mechanisms, making genetic models valuable for its study [1-4, 6-10].

In atherosclerosis, Tnc, especially its C domain/isoform (TNC-C), is strongly overexpressed in atherosclerotic plaque active areas. Delivery vectors recognizing TNC-C could be used for atherosclerosis-targeted drugs, and some conjugate agents are in clinical trials [1].

In cardiac injury after myocardial infarction, Tnc leads to cardiac fibrosis and cardiomyocyte apoptosis, and METTL3 enhances Tnc mRNA stability through m6A modification [2].

In gliomas, TDG-mediated active DNA demethylation upregulates Tnc, promoting glioma tumourigenesis [3].

In ankylosing spondylitis, Tnc promotes entheseal new bone formation by suppressing extracellular matrix adhesion force and activating Hippo signalling [4].

In myocardial ischemia/reperfusion injury, miR-495-3p targets Tnc to regulate cardiomyocyte apoptosis and inflammation [5].

In cancer, Tnc is a promising target for diagnostic and therapeutic approaches [6].

In melanoma, Tnc may be implicated in invasion and metastasis [7].

In diabetic kidney disease, Tnc promotes disease development through the TNC/TLR4/NF-κB/miR-155-5p inflammatory loop [8]. Also, serum Tnc levels could be a diagnostic biomarker for colorectal cancer [9].

In conclusion, Tnc is a multifunctional glycoprotein involved in numerous biological processes and diseases. Studies using genetic models, such as those related to Tnc in various disease conditions like atherosclerosis, cardiac injury, gliomas, etc., have revealed its significance in disease mechanisms. These findings contribute to understanding disease pathogenesis and developing potential therapeutic strategies.