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Axonal regeneration support refers to the collection of cellular and molecular mechanisms that enable neurons to regrow axons following injury. Regeneration can occur naturally in the peripheral nervous system (PNS) but is limited in the central nervous system (CNS) due to both extrinsic inhibitory cues (such as glial scarring and myelin-associated inhibitors) and intrinsic constraints on the neurons’ growth capacity. Key molecular pathways that support regeneration include increased transcriptional activity (via factors like c-Jun, STAT3, ATF3, and Smad1), activation of growth-associated signaling cascades (such as JAK/STAT, PI3K/Akt/mTOR), epigenetic remodelling (notably histone acetylation), cytoskeletal reorganization, and enhanced local energy metabolism (glycolysis and mitochondrial transport). Therapeutic strategies aim to reactivate these mechanisms (e.g., via gene therapy, drugs, or biomaterial scaffolds) to promote repair following spinal cord or brain injury[1][2][3][4][5][6].
Pathway activation (e.g., increasing cAMP, JAK/STAT, MAPK, mTOR signaling[2][5][6]); Inhibition of growth inhibitors (e.g., Rho/ROCK pathway[2][5]); Modulation of cytoskeletal dynamics; Epigenetic enhancement (histone acetylation[2][5])
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