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The cell regeneration process refers to the series of biological events through which cells are replaced or repaired to maintain or restore tissue function after injury or normal wear[1][2][4]. It is not a single molecule or receptor, but rather encompasses a broad array of cellular behaviors coordinated by multiple signaling pathways and cell types. This process includes activation of signaling cascades such as Wnt/β-catenin, Notch, PI3K/Akt, BMP, FGF, Hippo, Hedgehog, and TGF-β pathways, which collectively regulate cell proliferation, differentiation, apoptosis, and tissue patterning[1][3][5][6]. Stem cells—both embryonic and adult—play a fundamental role, providing a reservoir for new cells that replace those lost to injury or programmed cell death[1][4]. Regeneration can involve several mechanisms: - Proliferation of resident stem or progenitor cells, - Dedifferentiation/transdifferentiation of mature cells back into a more plastic state[4], - Programmed cell death (apoptosis) to sculpt and clear damaged tissue[3]. Disruptions in regeneration are implicated in diseases such as cancer (excess proliferation), degenerative disorders (insufficient regeneration), and fibrosis (maladaptive repair)[1]. Due to its process nature, "cell regeneration process" is not a specific druggable target, receptor, enzyme, or transporter, but a complex biological phenomenon involving multiple molecular targets and pathways[1][4][5]. For therapeutic or biomarker development, focus is typically placed on specific pathway members (e.g., Wnt receptors, Notch receptors, growth factors) rather than the overall process. Thus, for structured data, this entry is considered incorrect as a therapeutic target, but the underlying pathways and cellular actors are valid research and clinical targets.
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