アテローム性動脈硬化症: オープンアクセス

オープンアクセス

当社グループは 3,000 以上の世界的なカンファレンスシリーズ 米国、ヨーロッパ、世界中で毎年イベントが開催されます。 1,000 のより科学的な学会からの支援を受けたアジア および 700 以上の オープン アクセスを発行ジャーナルには 50,000 人以上の著名人が掲載されており、科学者が編集委員として名高い

オープンアクセスジャーナルはより多くの読者と引用を獲得
700 ジャーナル 15,000,000 人の読者 各ジャーナルは 25,000 人以上の読者を獲得

抽象的な

Vascular and Cardiac Valve Calcification in Chronic Kidney Disease

Lirong Hao, Xueying Chang, Yuting Fu and Zhangxiu He

Vascular calcification (VC) and cardiac valve calcification (CVC) are the important causes to increase the risk of cardiovascular events in terms of chronic kidney disease (CKD) patients. Once VC and CVC considered a passive form of dead or dying cells, it has now emerged as a pathology results from an active and highly regulated cellular process. Recently, mechanisms of VC have been further elucidated and many of the pathways involved could be amplified in CKD patients. In particular, FGF-23/Klotho axis, Wnt pathways, PI3K/Akt signaling, P38MAPK signaling pathway, and microRNAs have been shown to be impaired among patients with CKD and could play a role during vascular calcification. Furthermore, risks for CVC in CKD patients and molecular mechanisms related to it were verified by several researchers. The scope of the present review is to summarize the risk factors and pathophysiological mechanisms potentially involved in the link between CKD and the progression of VC and CVC.