title: MICS, an easily ignored contributor to arterial calcification in CKD patients.
abstract: In chronic kidney disease (CKD), simultaneous mineral and skeleton changes are prevalent, known as CKD-mineral bone disorder (CKD-MBD). Arterial calcification (AC) is a clinically important complication of CKD-MBD. It can increase arterial stiffness, which leads to severe cardiovascular events. However, current treatments have little effect on regression of AC, as its mechanisms are still unclear. There are multiple risk factors of AC, among which Malnutrition-Inflammation Complex Syndrome (MICS) is a new and crucial one. MICS, a combined syndrome of malnutrition and inflammation, generally begins at the early stage of CKD and becomes obvious in end-stage renal disease (ESRD). It was linked to reverse epidemiology and associated with increased cardiovascular mortality in ESRD patients. Recent data suggest that MICS can trigger CKD-MBD and accelerate the course of AC. In this present review, we summarize the recent understanding about the aggravating effects of MICS on AC and discuss the possible underlying mechanisms. A series of findings indicate that targeting MICS will provide a potential strategy for treating AC in CKD.
authors.affiliation: Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Department of Cardiology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Guangzhou, China.
authors.forename: Kun
authors.initials: K
authors.lastname: Zhang
authors.affiliation: Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Department of Cardiology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Guangzhou, China.
authors.forename: Jingwei
authors.initials: J
authors.lastname: Gao
authors.affiliation: Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Guangzhou, China; Department of Radiation Oncology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Chen
authors.affiliation: Division of Nephrology, Department of Internal Medicine, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China; and.
authors.forename: Xun
authors.initials: X
authors.lastname: Liu
authors.affiliation: Department of Medical Oncology, Sun Yat-sen University Cancer Center, SunYat-sen University, Guangzhou, China.
authors.forename: Qingqing
authors.initials: Q
authors.lastname: Cai
authors.affiliation: Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Department of Cardiology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Guangzhou, China.
authors.forename: Pinming
authors.initials: P
authors.lastname: Liu
authors.affiliation: Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Department of Cardiology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Guangzhou, China; huangh8@mail.sysu.edu.cn.
authors.forename: Hui
authors.initials: H
authors.lastname: Huang
mesh_terms: D006801:Humans; D007249:Inflammation / Q000150:complications*; D044342:Malnutrition / Q000150:complications*; D051436:Renal Insufficiency, Chronic / Q000150:complications*; D012307:Risk Factors; D013577:Syndrome; D061205:Vascular Calcification / Q000209:etiology*
keywords: arterial calcification; chronic kidney disease; chronic kidney disease-mineral bone disorder; malnutrition-inflammation complex syndrome; vascular smooth muscle cells