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The wound microenvironment components represent the intricate and dynamic assembly of cells, extracellular matrix (ECM) proteins, and biochemical signaling molecules that define the local site of tissue repair [5, 6]. This environment includes a variety of cell types such as neutrophils, macrophages, fibroblasts, and keratinocytes, which interact through a complex network of cytokines, growth factors like Vascular Endothelial Growth Factor (VEGF) and Platelet-Derived Growth Factor (PDGF), and matrix metalloproteinases (MMPs) [1, 3, 4]. In a healthy healing process, these components transition through coordinated phases of hemostasis, inflammation, proliferation, and remodeling to restore tissue integrity [2, 8]. However, in chronic or non-healing wounds, the microenvironment often becomes trapped in a state of persistent inflammation characterized by high levels of pro-inflammatory cytokines, excessive protease activity, and hypoxia [1, 7]. Therapeutic strategies targeting the wound microenvironment aim to correct these imbalances, often employing bioactive dressings, exogenous growth factors like Becaplermin, or antimicrobial agents to promote a transition toward the proliferative phase [4, 10]. Understanding the specific composition and state of the wound microenvironment is essential for the development of personalized regenerative medicine and advanced wound care therapies [7, 8].
Modulation of the inflammatory response by neutralizing pro-inflammatory cytokines or promoting M2 macrophage polarization; enzymatic debridement of necrotic tissue and degraded ECM to clear the wound bed; exogenous supplementation of growth factors to stimulate cell proliferation and angiogenesis; regulation of protease activity through MMP inhibition; antimicrobial action to reduce bioburden and disrupt biofilms.
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