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Complex multicellular immune and tissue repair networks represent the integrated systems of diverse cell types, including immune cells (such as macrophages and T cells) and stromal cells (such as fibroblasts and endothelial cells), that coordinate the response to tissue injury (Gurtner et al., 2008). These networks rely on a sophisticated exchange of biochemical signals, including cytokines, chemokines, and growth factors, to transition from an initial inflammatory phase to a proliferative and remodeling phase (Karin & Clevers, 2016). In healthy states, these networks ensure efficient wound healing and the restoration of tissue homeostasis. However, dysregulation of these interactions is a hallmark of various pathologies, including chronic non-healing wounds, systemic fibrosis, and the tumor microenvironment (Wynn & Vannella, 2016). Because these networks involve numerous redundant and pleiotropic pathways, they are typically addressed by targeting specific molecular nodes rather than the network as a single entity (Eming et al., 2017).
Modulation of specific cytokine signaling (e.g., TNF, IL-6, IL-1) or growth factor pathways (e.g., TGF-beta, VEGF) to resolve inflammation and prevent pathological scarring.
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