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Extracellular matrix–receptor interaction is not a molecule or receptor, but rather describes the broad collection of molecular interactions that occur between components of the extracellular matrix (ECM)—such as fibronectin, collagen, laminin—and a variety of cell-surface receptors, most notably **integrins**, as well as others (discoidin domain receptors, syndecans, CD44, RHAMM)[1][2][3][5]. These interactions are critical for cell anchorage, migration, signal transduction, proliferation, survival, and tissue homeostasis. Dysregulation of ECM–receptor interactions can contribute to diseases such as cancer, fibrosis, and impaired wound healing[2][3][5]. However, "extracellular matrix–receptor interaction" is a functional pathway or process and is not considered a specific therapeutic target, molecule, or receptor; instead, individual ECM proteins or receptors (e.g., integrins) are the actual molecular targets in drug discovery and therapeutic intervention[2][3][4]. **Note:** This entry is inappropriate as a molecular target, since it refers to a process or pathway rather than a discrete protein, enzyme, or receptor. Actual drug targeting focuses on the constituent molecules, such as specific integrin subunits, collagen types, or matrix metalloproteinases.
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