Timp4, or Tissue inhibitor of metalloproteinase 4, is a key regulator in various biological processes. It is involved in regulating the activity of matrix metalloproteinases (MMPs), which play a crucial role in extracellular matrix (ECM) remodeling. By modulating MMP activity, Timp4 influences processes like cell migration, tissue repair, and angiogenesis. It is also associated with signaling pathways such as ER-α, HIF1A, TGF-β, and FOXO3 in breast cancer cells [3].

In mouse models, the loss of Timp4 does not exacerbate thoracic and abdominal aortic aneurysm severity, unlike TIMP3 loss [1]. In Timp4-deficient rats, a series of ocular morphology abnormalities occur in a dose-dependent manner, including retinal thickness decline, axial length elongation, and sclera and retina collagen content decrease, suggesting its role in ocular development [2]. In atherosclerotic mouse models, loss of Timp4 promotes atherosclerotic plaque deposition in the abdominal aorta despite suppressed plasma cholesterol levels [4].

In conclusion, Timp4 plays significant roles in maintaining the balance of ECM remodeling, influencing ocular development, and having an impact on atherosclerotic plaque formation. The study of Timp4 gene knockout mouse models has provided valuable insights into its functions in these disease-related processes, helping to further understand the underlying mechanisms and potentially develop new therapeutic strategies for related diseases.