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首页> 外文期刊>Kidney international supplements. >A phosphate-centric paradigm for pathophysiology and therapy of chronic kidney disease
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A phosphate-centric paradigm for pathophysiology and therapy of chronic kidney disease

机译：一种以磷生理学和慢性肾病治疗为中心的范式范式

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Extracellular phosphate is toxic to the cell at high concentrations. When the phosphate level is increased in the blood by impaired urinary phosphate excretion, premature aging ensues. When the phosphate level is increased in the urine by dietary phosphate overload, this may lead to kidney damage (tubular injury and interstitial fibrosis). Extracellular phosphate exerts its cytotoxicity when it forms insoluble nanoparticles with calcium and fetuin-A, referred to as calciprotein particles (CPPs). CPPs are highly bioactive ligands that can induce various cellular responses, including osteogenic transformation of vascular smooth muscle cells and cell death in vascular endothelium and renal tubular epithelium. CPPs are detected in the blood of animal models and patients with chronic kidney disease (CKD) and associated with adaptation of the endocrine axes mediated by fibroblast growth factor-23 (FGF23) and Klotho that regulate mineral metabolism and aging. These observations have raised the possibility that CPPs may contribute to the pathophysiology of CKD. This notion, if validated, is expected to provide new diagnostic and therapeutic targets for CKD.
机译：细胞外磷酸盐在高浓度下对细胞有毒。当血液中磷酸盐水平增加时，通过受损的尿磷酸盐排泄，随后会发生过早。当尿液磷酸盐过载在尿液中磷酸盐水平增加时，这可能导致肾脏损伤（管状损伤和间质纤维化）。当用钙和胎素-A形成不溶性纳米颗粒时，细胞外磷酸盐施加其细胞毒性，称为CAPIPROTEIN颗粒（CPP）。 CPP是高度生物活性配体，可诱导各种细胞反应，包括血管平滑肌细胞和血管内皮和肾小管上皮细胞死亡的骨性转化。在动物模型的血液和慢性肾病（CKD）患者中检测到CPP，并与成纤维细胞生长因子-33（FGF23）和Klotho介导的内分泌轴和调节矿物代谢和老化的肺炎的适应相关。这些观察结果提出了CPP可能导致CKD的病理生理学有助于促进CKD的可能性。如果验证，这一概念预计将为CKD提供新的诊断和治疗目标。

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