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Wound bed stromal and parenchymal cells encompass the diverse cellular components essential for the physiological process of tissue repair following injury. Stromal cells, including fibroblasts, pericytes, and endothelial cells, form the supportive framework and vasculature, while parenchymal cells, such as keratinocytes in the epidermis, perform the primary functional roles of the tissue (Gurtner et al., 2008, Nature [https://www.nature.com/articles/nature07039]). These cells are not a single molecular target but rather a coordinated biological system that responds to various therapeutic interventions, such as growth factors and specialized dressings, to facilitate wound closure (Werner & Grose, 2003, Physiological Reviews [https://journals.physiology.org/doi/full/10.1152/physrev.00031.2002]). In chronic conditions like diabetic ulcers, the dysfunction of these cells—characterized by impaired migration and excessive senescence—leads to healing arrest (Velnar et al., 2009, Journal of International Medical Research [https://journals.sagepub.com/doi/10.1177/147323000903700531]). Therapeutic strategies often aim to stimulate these cells using agents like Becaplermin, which mimics endogenous signaling to promote proliferation and extracellular matrix deposition (Papanas & Maltezos, 2007, Clinical Interventions in Aging [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2684071/]). Understanding the interplay between these cell types is crucial for developing treatments for both non-healing wounds and fibroproliferative disorders.
Stimulation of cellular proliferation, migration, and extracellular matrix production through growth factor signaling and enzymatic debridement of necrotic tissue.
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