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Different Types of Iron Deficiency
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<blockquote data-quote="madman" data-source="post: 208496" data-attributes="member: 13851"><p><strong>Figure 1:<u> Coordinated homoeostatic response to absolute and functional iron deficiency</u> Red arrows refer to physiological stimuli (eg, absolute iron deficiency or increased erythropoiesis) that suppress hepcidin expression. <u>During absolute iron deficiency, decreased circulating transferrin saturation and liver iron storage suppress hepcidin transcription via reduced BMP-SMAD signalling</u> (<u>yellow pathway</u>). As a consequence, duodenal and macrophage FPN proteins are stabilised, facilitating dietary iron absorption in duodenal enterocytes and release of iron from macrophages of the reticuloendothelial system, thereby increasing iron concentrations in the plasma. Additionally, reduced iron concentration in duodenal enterocytes is sensed by the iron-dependent prolyl hydroxylase domain enzymes that increase the stability of the transcription factor HIF-2, which regulates transcription of apical (CYBRD1 and DMT1) and basolateral (FPN) iron transport machinery. During iron deficiency, in most cell types the IRP/IRE system stabilises mRNAs of proteins crucial for iron uptake (eg, TfR1 and DMT1) and suppresses the synthesis of proteins involved in the storage (ferritin), utilisation (cytoplasmic and mitochondrial iron-containing proteins), and export (FPN) of iron.<u> In functional iron deficiency, inflammation increases hepatic hepcidin expression via IL6-JAK2-STAT3 signalling</u> (<u>green pathway</u>), <u>causing reduced FPN abundance and function on cells, depriving the plasma of iron</u>. In response to iron deficiency anaemia, the kidney produces erythropoietin, which stimulates erythropoiesis. Erythroblast erythropoietin sensitivity can be modulated by TfR2. <u>In absolute iron deficiency, erythroblasts and erythrocytes donate iron through FPN-mediated iron export</u>. <u>Increased erythropoiesis (eg, during recovery from anaemia) causes secretion of erythroferrone, which suppresses hepatic hepcidin expression via inhibition of BMP-SMAD signalling</u> (<u>red pathway</u>). LSEC=liver sinusoidal endothelial cell. P=phosphorylated. TSAT=transferrin saturation.</strong></p><p><strong>[ATTACH=full]16645[/ATTACH]</strong></p></blockquote><p></p>
[QUOTE="madman, post: 208496, member: 13851"] [B]Figure 1:[U] Coordinated homoeostatic response to absolute and functional iron deficiency[/U] Red arrows refer to physiological stimuli (eg, absolute iron deficiency or increased erythropoiesis) that suppress hepcidin expression. [U]During absolute iron deficiency, decreased circulating transferrin saturation and liver iron storage suppress hepcidin transcription via reduced BMP-SMAD signalling[/U] ([U]yellow pathway[/U]). As a consequence, duodenal and macrophage FPN proteins are stabilised, facilitating dietary iron absorption in duodenal enterocytes and release of iron from macrophages of the reticuloendothelial system, thereby increasing iron concentrations in the plasma. Additionally, reduced iron concentration in duodenal enterocytes is sensed by the iron-dependent prolyl hydroxylase domain enzymes that increase the stability of the transcription factor HIF-2, which regulates transcription of apical (CYBRD1 and DMT1) and basolateral (FPN) iron transport machinery. During iron deficiency, in most cell types the IRP/IRE system stabilises mRNAs of proteins crucial for iron uptake (eg, TfR1 and DMT1) and suppresses the synthesis of proteins involved in the storage (ferritin), utilisation (cytoplasmic and mitochondrial iron-containing proteins), and export (FPN) of iron.[U] In functional iron deficiency, inflammation increases hepatic hepcidin expression via IL6-JAK2-STAT3 signalling[/U] ([U]green pathway[/U]), [U]causing reduced FPN abundance and function on cells, depriving the plasma of iron[/U]. In response to iron deficiency anaemia, the kidney produces erythropoietin, which stimulates erythropoiesis. Erythroblast erythropoietin sensitivity can be modulated by TfR2. [U]In absolute iron deficiency, erythroblasts and erythrocytes donate iron through FPN-mediated iron export[/U]. [U]Increased erythropoiesis (eg, during recovery from anaemia) causes secretion of erythroferrone, which suppresses hepatic hepcidin expression via inhibition of BMP-SMAD signalling[/U] ([U]red pathway[/U]). LSEC=liver sinusoidal endothelial cell. P=phosphorylated. TSAT=transferrin saturation. [ATTACH type="full"]16645[/ATTACH][/B] [/QUOTE]
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Different Types of Iron Deficiency
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