Atherosclerosis ; etiology ; metabolism ; Humans ; Inflammation

Atherosclerosis ; complications ; Erectile Dysfunction ; etiology ; Humans ; Male

Air Pollution ; Atherosclerosis ; etiology ; Humans ; Particulate Matter

Atherosclerosis ; etiology ; therapy ; Humans ; Lupus Erythematosus, Systemic ; pathology ; therapy

OBJECTIVETo review the recent research progress in lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) including its protein, ligands, expression and pathophysiological significance. Data sources Information included in this article was identified by searching of PUBMED (1997 - 2006) online resources using the key term LOX-1.

STUDY SELECTIONMainly original milestone articles and critical reviews written by major pioneer investigators of the field were selected.

RESULTSThe key issues related to the LOX-1 protein as well as ligands for LOX-1. Factors regulating the expression of LOX-1 were summarized. The pathophysiological functions of LOX-1 in several diseases were discussed.

CONCLUSIONSIdentification of LOX-1 and a definition of its biological role in pathophysiologic states provide deeper insight into the pathogenesis of some cardiovascular diseases especially in atherosclerosis and provide a potential selective therapeutic approach. LOX-1 is unlocking and drugs targeting LOX-1 might be a promising direction to explore.

Animals ; Arthritis, Rheumatoid ; etiology ; Atherosclerosis ; etiology ; Humans ; Ligands ; Myocardial Infarction ; etiology ; Osteoarthritis ; etiology ; Scavenger Receptors, Class E ; chemistry ; genetics ; physiology

OBJECTIVETo evaluate whether glycation of high-density lipoprotein (HDL) increases cardiovascular risk in patients with type 2 diabetes mellitus by altering its anti-atherogenic property.

DATA SOURCESData cited in this review were obtained mainly from Pubmed and Medline in English from 2000 to 2013, with keywords "glycation", "HDL", and "atherosclerosis". Study selection Articles regarding glycation of HDL and its role in atherogenesis in both humans and experimental animal models were identified, retrieved and reviewed.

RESULTSGlycation alters the structure of HDL and its associated enzymes, resulting in an impairment of atheroprotective functionality and increased risks for cardiovascular events in type 2 diabetic patients.

CONCLUSIONGlycation of HDL exerts a deleterious effect on the development of cardiovascular complications in diabetes.

Atherosclerosis ; etiology ; metabolism ; Cardiovascular Diseases ; etiology ; metabolism ; Diabetes Mellitus, Type 2 ; complications ; metabolism ; Humans ; Lipoproteins, HDL

BACKGROUNDThe expression of TES, a novel tumor suppressor gene, is found to be down-regulated in the left anterior descending aorta of patients with coronary artery disease (CAD) compared with non-CAD subjects. This study aimed to investigate the expression of TES during the development of atherosclerosis in rabbits.

METHODSThirty-two New Zealand rabbits were randomly divided into a normal diet (ND) and high-fat diet (HFD) groups. Body weight and serum lipid levels were measured at 0, 4, and 12 weeks after diet treatment. The degree of atherosclerosis in thoracic aortas was analyzed by histological examinations. The expression of Testin in the tissue samples was inspected via immunohistochemical and immunofluorescence confocal microscopy. Real time-polymerase chain reaction and Western blot analysis were performed to evaluate the expression of TES/Testin at mRNA and protein levels in the aortic tissues.

RESULTSAfter 12 weeks postenrollment, rabbits in HFD group had a higher level of serum lipids and atherosclerotic plaque compared to ND group (P < 0.05). Testin expression was detected at high levels in the endothelium and a weak expression on the subendothelium area. The expression of TES mRNA was markedly reduced by 10-fold in the aortic tissues in the HFD group compared with the ND group (P = 0.015), and the protein level was also significantly decreased in the HFD group (P < 0.05).

CONCLUSIONSReduced TES/Testin expression is associated with the development of atherosclerosis, implicating a potentially important role in the pathogenesis of atherosclerosis.

Animals ; Aorta ; metabolism ; Atherosclerosis ; etiology ; metabolism ; Diet, High-Fat ; adverse effects ; Proteins ; genetics ; metabolism ; Rabbits

Atherosclerosis ; etiology ; pathology ; Coronary Angiography ; Humans ; Myocardial Bridging ; diagnosis ; epidemiology ; physiopathology

OBJECTIVETo establish the distribution of 10-year atherosclerotic cardiovascular disease (ASCVD) risk among Chinese adults.

METHODSWe estimated the 10-year ASCVD risk by applying the 2013 American College of Cardiology/ American Heart Association pooled cohort equations (PCEs) to the data obtained from the 2010 China Chronic Disease and Risk Factor Surveillance that involved 61,541 participants (representing 520,158,652 Chinese adults) aged 40-79 years. We also compared the ASCVD risk with the 10-year ischemic cardiovascular disease (ICVD) risk, which was calculated using the simplified scoring tables recommended by the Chinese Guidelines for Prevention of Cardiovascular Diseases (Chinese model).

RESULTSBased on the PCEs, the average 10-year ASCVD risk among adults without self-reported stroke or myocardial infraction was 12.5%. Approximately 247 million (47.4%) and 107 million (20.6%) adults had ⋝ 7.5% and > 20% 10-year ASCVD risks, respectively. The 10-year ASCVD risk > 20% was higher among men, less educated individuals, smokers, drinkers, and physically inactive individuals than among their counterparts. Overall, 29.0% of adults categorized using the Chinese model were overclassified with the PCEs.

CONCLUSIONOur results define the distribution of 10-year ASCVD risk among Chinese adults. The 10-year ASCVD risk predicted by the PCEs was higher than the ICVD risk predicted by the Chinese model.

Adult ; Aged ; Atherosclerosis ; epidemiology ; etiology ; China ; epidemiology ; Female ; Humans ; Male ; Middle Aged ; Risk Assessment ; Risk Factors

Animals ; Atherosclerosis ; etiology ; genetics ; pathology ; China ; Coronary Disease ; pathology ; Genes, p53 ; Humans ; Point Mutation ; Risk Factors