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Ca2+ homeostasis in microvascular endothelial cells from an insulin-dependent diabetic model: role of endosomes/lysosomes

机译:胰岛素依赖型糖尿病模型中微血管内皮细胞中的Ca2 +稳态:内体/溶酶体的作用

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Abstract: Cytosolic Ca$+2$PLU$/ ($LB@Ca$+2$PLU$/$RB$+cyt$/) regulates several cellular functions, e.g. cell growth, contraction, secretion, etc. In many cell types, ion homeostasis appears to be coupled with glucose metabolism. In certain cell types, a strict coupling between glycolysis and the activity of Sarcoplasmic/Endoplasmic Reticulum Ca$+2$PLU$/-ATPases (SERCA) has been suggested. Glucose metabolism is altered in diabetes. We hypothesize that: (1) Ca$+2$PLU$/ homeostasis is altered in microvascular endothelial cells from diabetic animals due to the dysfunction of glycolysis coupling the activity of SERCA; (2) endosomal/lysosomal compartments expressing SERCA are involved in the dysfunction associated with diabetes.!50
机译:摘要:胞质Ca $ + 2 $ PLU $ /($ LB @ Ca $ + 2 $ PLU $ / $ RB $ + cyt $ /)调节多种细胞功能,例如细胞生长,收缩,分泌等。在许多细胞类型中,离子稳态似乎与葡萄糖代谢有关。在某些细胞类型中,已提出糖酵解与肌浆/内质网Ca $ + 2 $ PLU $ /-ATPases(SERCA)活性之间的严格耦合。糖尿病患者的葡萄糖代谢发生改变。我们假设:(1)糖尿病动物的微血管内皮细胞中Ca $ + 2 $ PLU $ /稳态发生改变,这是由于糖酵解功能障碍与SERCA的活性有关; (2)表达SERCA的内体/溶酶体区室参与了与糖尿病相关的功能障碍!50

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