{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nZIP14 (encoded by SLC39A14) is a multifaceted transmembrane metal‐ion transporter that localizes to the plasma membrane and endosomal compartments, mediating the cellular uptake of essential metal ions such as zinc, ferrous iron, and manganese, as well as toxic metals like cadmium. It not only facilitates the import of zinc under basal conditions but also enables non–transferrin‐bound iron (NTBI) uptake, with its activity markedly enhanced upon proinflammatory stimulation (e.g., via IL-6), thereby linking inflammation to alterations in metal metabolism. This transporter exhibits saturable and substrate‐specific kinetics with dependencies on co‐ions (such as Ca2+ or HCO3–), and its expression can be dynamically regulated during acute-phase responses and inflammatory insults."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n\n"}]}, {"type": "t", "text": "\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its canonical role in metal uptake, ZIP14 helps coordinate systemic metal homeostasis and cellular responses during disease. In hepatocytes, ZIP14 contributes to hepatic iron loading in conditions such as hemochromatosis by mediating NTBI uptake, while also influencing zinc redistribution during inflammatory states, which may affect GPCR-mediated signaling and systemic growth. Additionally, in contexts like the kidney and intestine, ZIP14 regulates not only metal absorption and excretion but also modulates epithelial barrier function and immune responses—processes that impact metabolic disorders, inflammatory bowel conditions, and adipose tissue function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "15"}]}, {"type": "t", "text": "\n\n"}]}, {"type": "t", "text": "\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMoreover, the role of ZIP14 in manganese handling has emerged as crucial, with deficiencies in its function leading to impaired manganese uptake by the liver and pancreas, subsequent systemic and brain manganese accumulation, and neurotoxicity manifesting as motor deficits and dystonia-parkinsonism. These studies further indicate that ZIP14-mediated transport is indispensable for preventing abnormal metal accumulation in critical tissues, and its dysregulation has downstream effects on energy metabolism, insulin signaling, and even epigenetic regulation of inflammatory gene networks within the gut. Collectively, the breadth of these findings implicates ZIP14 as a central regulator of metal-ion homeostasis, with profound effects on metabolic, hepatic, intestinal, and neurological functions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "16", "end_ref": "30"}]}, {"type": "t", "text": "\n\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Juan P Liuzzi, Louis A Lichten, Seth Rivera, et al. 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