Ecm1, or extracellular matrix protein 1, is a key protein that interacts with extracellular and structural proteins. It plays essential roles in maintaining the extracellular matrix and is associated with multiple biological pathways, such as those related to cell adhesion, growth, and differentiation. Genetic models, like gene knockout mice, have been crucial for studying its functions [2,3].

In liver-related studies, Ecm1-knockout (ECM1-KO) mice spontaneously developed liver fibrosis and died by 2 months of age without significant hepatocyte damage or inflammation, indicating that Ecm1 inhibits activation of TGF-β and hepatic stellate cells (HSCs) to prevent fibrogenesis [2]. In hepatocyte-specific Ecm1-deficient mice, the antifibrotic effect of salvianolic acid B was abolished, suggesting Ecm1 is a target for salvianolic acid B in alleviating liver fibrosis by inhibiting hepatocyte ferroptosis [1]. Also, overexpression of ECM1 in hepatic stellate cells (HSCs) prevented latent TGF-β1 (LTGF-β1) activation mediated by thrombospondins (TSPs), ADAMTS proteases, and matrix metalloproteinases (MMPs), and in mice, ECM1 overexpression attenuated KRFK-induced LTGF-β1 activation [3].

In conclusion, Ecm1 is vital in preventing liver fibrosis by maintaining TGF-β in its latent form and inhibiting HSC activation. Gene-knockout mouse models have significantly contributed to understanding its role in liver-related diseases, offering potential therapeutic targets for treating liver fibrosis [1,2,3].