CCN1, previously named CYR61 (cysteine-rich angiogenic inducer 61), belongs to the CCN family of matricellular proteins. It plays critical roles in regulating proliferation, differentiation, apoptosis, angiogenesis, and fibrosis. CCN1 is positively regulated by TGF-beta and the hippo/YAP/TAZ mechanotransduction pathway [1,2].

In fibroblast-specific CCN1-deficient mice, there was progressive skin thinning, reduced accumulation of type I collagen, and resistance to bleomycin-induced skin fibrosis, suggesting CCN1 expression by fibroblasts is essential for skin fibrosis [5]. In ConA-induced hepatitis mice model, CCN1 conditional knockout attenuated inflammation by reducing ALT/AST level and IL-6 expression, indicating CCN1 promotes inflammation in autoimmune hepatitis [4]. In EC-specific CCN1 gene-deleted mice, it mimicked a YAP gain-of-function phenotype with EC hyperproliferation and blood vessel enlargement, highlighting its role in angiogenesis [3].

In conclusion, CCN1 is crucial for various biological processes such as angiogenesis, inflammation, and fibrosis. Gene-knockout and conditional-knockout mouse models have revealed its significant contributions to diseases like skin fibrosis, autoimmune hepatitis, and neovascular diseases, providing valuable insights into its functions and potential as a therapeutic target.