Vascular calcification in chronic kidney disease: pathogenesis and clinical implications.
Vascular calcification in chronic kidney disease: pathogenesis and clinical implications.
复制标题
慢性肾脏病的血管钙化：发病机制和临床意义。
DOI：
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发表时间：
2009
影响因子：
3.2
通讯作者：
Y. Nishizawà
中科院分区：
文献类型：
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作者：
A. Shioi;Y. Nishizawà
心血管疾病是慢性肾脏疾病(CKD)发病率和死亡率的主要原因。非传统尿毒症相关危险因素和传统危险因素可能共同导致CKD患者心血管疾病的独特特征。血管钙化是慢性肾脏病动脉疾病的一个显著特征，可能通过调节动脉硬化(动脉硬化)和动脉粥样硬化来影响心血管死亡率。血管钙化的发生有两个病理生理过程：细胞凋亡和向软骨细胞或成骨细胞的表型转变(软骨/成骨分化)。在慢性肾脏病中，矿物质代谢异常，主要是高磷血症和高钙血症，促进了血管钙化的进展，并伴随着其抑制分子(血管钙化抑制物)的功能障碍，如焦磷酸、基质GLA蛋白、胎球蛋白-A和护骨素。
Cardiovascular disease is the primary cause of morbidity and mortality in chronic kidney disease (CKD). Nontraditional uremia-related risk factors as well as traditional risk factors may contribute to the unique features of cardiovascular disease in patients with CKD. Vascular calcification is a prominent feature of arterial disease in CKD and may have an impact on cardiovascular mortality through modulating both arteriosclerosis (arterial stiffening) and atherosclerosis. There are two pathophysiological processes involved in the development of vascular calcification: apoptosis and phenotypic transition to chondrocytes or osteoblasts (chodro/osteogenic differentiation). In CKD, abnormal mineral metabolism, predominantly hyperphosphatemia and hypercalcemia, facilitates progression of vascular calcification in association with functional disturbances of its inhibitory molecules (inhibitors of vascular calcification) such as pyrophosphate, matrix Gla protein, fetuin-A, and osteoprotegerin.
影响因子：
19.6
作者：
Lomashvili, K. A.;Garg, P.;O'Neill, W. C.
通讯作者：
O'Neill, W. C.