Kuroo Makoto
Division of Anti-aging Medicine, Center for Molecular Medicine, Jichi Medical University, Japan.
Clin Calcium. 2014 Dec;24(12):1785-92.
Phosphate restriction has been shown to improve clinical outcomes in patients with chronic kidney disease (CKD) . However, the molecular mechanism underlying the harm in phosphate overload remains unclear. Recent studies suggest that the true culprit of phosphate toxicity may not be phosphate per se but calciprotein particles (CPPs) , colloidal nanoparticles composed of calcium phosphate crystals and mineral binding proteins such as Fetuin-A. CPPs are highly bioactive ligands that induce cell damage and innate immune responses. Serum levels of CPPs are increased in CKD patients and independently associated with vascular calcification and chronic inflammation. CPPs may be viewed as a "pathogen" that plays an important role in the pathophysiology of CKD.
已证明限制磷摄入可改善慢性肾脏病(CKD)患者的临床结局。然而,磷过载造成损害的分子机制仍不清楚。最近的研究表明,磷毒性的真正元凶可能不是磷本身,而是钙蛋白颗粒(CPPs),它是由磷酸钙晶体和诸如胎球蛋白-A等矿物质结合蛋白组成的胶体纳米颗粒。CPPs是诱导细胞损伤和先天性免疫反应的高生物活性配体。CKD患者血清中CPPs水平升高,并与血管钙化和慢性炎症独立相关。CPPs可被视为在CKD病理生理学中起重要作用的“病原体”。