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"Neuronal regeneration pathways" encompass the diverse signaling systems and transcriptional programs that govern the intrinsic and extrinsic response of neurons to injury, directing axonal regrowth, dendritic plasticity, and, in some cases, neurogenesis. These involve growth factor signaling (e.g., FGF, WNT, PDGF, BDNF), mitogen-activated protein kinase (MAPK) cascades (e.g., JNK, p38), cAMP response elements, PI3K/Akt/mTOR pathway, JAK/STAT signaling, semaphorin-plexin and integrin-mediated networks, and are regulated both at the level of transcription (by factors such as ATF3, KLF family) and cytoskeleton dynamics (through proteins like CRMP2, CLASP, tau). The pathways are targets for modulating repair after central and peripheral nervous system damage, but due to their broad physiological roles, direct pharmacological targeting involves safety concerns such as cancer risk or maladaptive plasticity (e.g., pain syndromes) [1][2][3][4][5][6]. In summary, "Neuronal regeneration pathways" is not a specific, targetable molecule or protein but a conceptual category encompassing a large, complex set of repair-associated signaling mechanisms in the nervous system.
Growth factor receptor agonism (e.g., BDNF/TrkB); MAPK/ERK pathway activation; JAK/STAT pathway activation; PI3K/Akt/mTOR enhancement; RhoA/ROCK inhibition; GSK3β inhibition
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