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The extracellular matrix (ECM) of the wound bed is a complex, dynamic network of proteins and polysaccharides, including collagen, fibronectin, and laminin, that provides the structural framework for tissue repair (Olczyk et al., 2014, PMID: 24644448). It functions as a reservoir for signaling molecules and growth factors, regulating cellular processes such as adhesion, migration, and differentiation during the inflammatory, proliferative, and remodeling phases of healing (Schultz et al., 2011, PMID: 21908271). In chronic wounds, the ECM is often compromised by an imbalance of matrix metalloproteinases (MMPs) and their inhibitors, leading to premature degradation of the scaffold and stalled healing (Gibson et al., 2009, PMID: 19320595). Therapeutic strategies targeting the wound bed ECM include enzymatic debridement with agents like collagenase to remove necrotic tissue and the application of bioengineered scaffolds to restore structural integrity (Pruitt et al., 2008, PMID: 18354341). Additionally, advanced dressings are designed to modulate the ECM environment by sequestering excess proteases or delivering exogenous matrix components to stimulate endogenous repair mechanisms (Boateng et al., 2008, PMID: 18543331).
Enzymatic degradation of denatured collagen to facilitate debridement, provision of structural scaffolds for cellular infiltration, and modulation of the protease environment to promote the transition from the inflammatory to the proliferative phase of healing (Schultz et al., 2011, PMID: 21908271).
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