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The extracellular matrix (ECM) in liver tissue is a complex network of macromolecules—primarily collagens, glycoproteins, proteoglycans, and various associated proteins—that provides structural scaffolding and regulates cellular behavior, including adhesion, migration, proliferation, differentiation, and immune response[5][1][4][3][7]. In healthy liver, the ECM is limited and dynamically regulated; in pathological states such as chronic injury or cirrhosis, excessive ECM deposition and altered composition disrupt normal architecture, leading to fibrosis, inflammation, and impaired function[2][4][6][7]. While ECM components, such as specific collagens or glycoproteins, may serve as drug targets and diagnostic biomarkers, "extracellular matrix deposition" itself is a process, not a molecular entity or canonical therapeutic target. Note: The entry "Extracellular matrix deposition in liver tissue" is not a molecular target (e.g., receptor or enzyme) but describes a phenomenon/process. When targeting therapeutic interventions, specific ECM constituents (e.g., collagen type I, matrix metalloproteinases) or their biosynthetic/modulatory pathways are considered true molecular targets[3][5][6].
Drugs affecting ECM deposition typically act through inhibition of ECM synthesis, promotion of ECM degradation (e.g., by upregulating matrix metalloproteinases), or modulation of collagen deposition.
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