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Is inflammation the link between atherosclerosis and vascular calcification in chronic kidney disease?

机译:炎症是慢性肾脏疾病中动脉粥样硬化与血管钙化之间的联系吗?

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摘要

Atherosclerosis and vascular calcification often co-exist in chronic kidney disease (CKD) patients. Although the former has been recently recognized as an active inflammatory process, atherosclerosis-related calcification of the intima is still viewed as a passive epiphenomenon. Recent experimental data showed that ossification of the internal vascular wall might also be an active inflammatory process interrelated to atherosclerosis. Factors like RANKL (receptor activator of nuclear factor kappaB ligand), RANK and osteoprotegerin modulate vascular calcification and at the same time are involved in the process of atherosclerosis. Moreover, basic calcium phosphate crystals could interact with and activate monocytes-macrophages that produce proinflammatory cytokines capable of initiating - via endothelial activation and leukocyte adhesion - the atherosclerotic process. Thus, vascular calcification might be an active player and not simply an epiphenomenon in atherosclerosis. Should the above-mentioned databe confirmed in future studies, calcification of the internal vascular wall and atherosclerosis might be viewed and treated as tightly interconnected and linked by inflammation processes in CKD patients.
机译:慢性肾病(CKD)患者通常并存动脉粥样硬化和血管钙化。尽管前者最近被认为是主动的炎症过程,但动脉粥样硬化相关的内膜钙化仍被视为被动的现象。最近的实验数据表明,血管内壁的骨化也可能是与动脉粥样硬化相关的活跃的炎症过程。像RANKL(核因子kappaB配体的受体激活剂),RANK和骨保护素之类的因子可调节血管钙化,同时也参与动脉粥样硬化的进程。此外,碱性磷酸钙晶体可以与单核细胞-巨噬细胞相互作用并激活单核细胞-巨噬细胞,所述单核细胞-巨噬细胞能够通过内皮激活和白细胞粘附来启动动脉粥样硬化过程。因此,血管钙化可能是一个活跃的参与者,而不仅仅是动脉粥样硬化的一种表象现象。如果上述数据在以后的研究中得到证实,则可以将CKD患者的炎症过程视为血管内壁钙化和动脉粥样硬化的紧密联系和联系。

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