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Morphogens represent a diverse functional class of signaling molecules that orchestrate the spatial organization and patterning of tissues during embryonic development and adult regeneration [1, 4]. These molecules operate by forming extracellular concentration gradients; cells interpret their local concentration to activate specific gene expression programs, thereby determining their developmental fate [3, 6, 7]. Key mammalian morphogen families include Hedgehog (Hh), Wingless-related (Wnt), Transforming growth factor-beta (TGF-β), and Bone morphogenetic proteins (BMPs) [4, 5, 10]. In adult physiology, dysregulation or reactivation of these developmental pathways is frequently implicated in pathologies such as cancer, where they drive tumor growth, and fibrosis, where they promote myofibroblast activation [2, 11]. Therapeutic strategies involve the use of small molecules or biologics to either inhibit overactive signaling, as seen with Hedgehog inhibitors in basal cell carcinoma, or to stimulate regenerative processes, such as the use of recombinant BMPs in orthopedic surgery [5, 9, 11].
Regulation of signal transduction through concentration-dependent binding to specific cell-surface receptors (e.g., Patched, Frizzled, TGF-beta receptors), leading to the stabilization of intracellular mediators and differential gene transcription [4, 6, 8].
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