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Physical wound closure refers to the process by which the edges of a wound are brought together and the gap is closed, restoring tissue integrity. This phenomenon is primarily orchestrated by the coordinated activity of multiple cell types—including keratinocytes, fibroblasts, myofibroblasts, macrophages, and endothelial cells—along with the remodeling of the extracellular matrix[1][3][4][5]. Key mechanisms include *keratinocyte migration* (re-epithelialization), *fibroblast-driven ECM deposition*, and especially *wound contraction* driven by myofibroblasts, which develop contractile structures and physically draw wound edges together[1][3][4][5]. Mechanical forces (e.g., actomyosin cables), cellular migration, and ECM cross-linking all contribute to the rapid and effective closure of tissue gaps[2][4][5][7]. This process is essential for early tissue repair but can become pathological in cases of excessive scarring or failure to close (chronic wounds). Summary: "Physical wound closure" is not a druggable target but rather a process; any entry of this as a "target" in a therapeutic database should be flagged as problematic. Underlying *cellular and molecular drivers* of wound closure—such as the TGF-β pathway, myofibroblast activity, and integrins—are true targets for therapeutic intervention[1][3][4].
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