Atherosclerosis ; complications ; pathology ; Humans ; Thrombosis ; complications ; pathology

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

Atherosclerosis ; Humans ; Polysomnography ; Sleep Apnea, Obstructive/complications*

Atherosclerosis ; complications ; epidemiology ; Carotid Artery Diseases ; complications ; epidemiology ; Glucose Metabolism Disorders ; complications ; epidemiology ; Humans ; Tibet ; epidemiology

Atherosclerosis ; complications ; Fatty Liver ; complications ; Humans ; Non-alcoholic Fatty Liver Disease

Hyperhomocysteinemia (HHcy) has been recognized as an independent risk factor for atherosclerosis for more than 30 years, but the mechanisms by which HHcy leads to atherosclerosis are not well fully understood. In this review, we will summarize the immunoregulatory effects of homocysteine on cardiovascular diseases from humoral immunity, monocyte/macrophage and T lymphocyte activity. Homocysteine can induce chemokine and cytokine secretion in monocytes and T lymphocytes and also directly stimulate B lymphocyte proliferation and IgG secretion. In addition, the cellular mechanisms that may explain the pro-inflammatory effect of HHcy are included. Homocysteine may directly or indirectly lead to oxidative stress or endoplasmic reticulum (ER) stress. Elevated levels of homocysteine also decrease the bioavailability of nitric oxide and modulate the levels of other metabolites including S-adenosyl methionine and S-adenosyl homocysteine which may result in cardiovascular diseases.
Animals ; Atherosclerosis ; Cardiovascular Diseases ; immunology ; physiopathology ; Homocysteine ; physiology ; Humans ; Hyperhomocysteinemia ; complications ; Macrophages ; Nitric Oxide ; Oxidative Stress

The high incidence of atherosclerosis and cardiovascular disease is the leading cause of morbidity and mortality among diabetic patients. It is well known that postprandial hyperglycemia is an independent risk factor for diabetic complications and mortality. For better management of diabetic patients, effort must be put forth to not only achieve the HbA1c target, but also to control postprandial hyperglycemia. This article reviews the pathophysiology and clinical aspects of postprandial hyperglycemia to appropriately control blood glucose level.
Atherosclerosis ; Blood Glucose ; Cardiovascular Diseases ; Diabetes Complications ; Hemoglobin A, Glycosylated ; Humans ; Hyperglycemia ; Incidence ; Risk Factors

Atherosclerosis ; complications ; pathology ; Blood Platelets ; physiology ; Humans ; Platelet Activation ; Thrombosis ; etiology ; pathology

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

Hyperhomocysteinemia (HHcy) is considered to be an independent risk factor for cardiovascular diseases, but the molecular mechanisms underlying its pathogenesis are not fully understood. Endothelial dysfunction is a key initiating factor in the pathogenesis of atherosclerosis, which is commonly observed in almost all HHcy-induced vascular diseases. HHcy promotes oxidative stress, inhibits nitric oxide production, suppresses hydrogen sulfide signaling pathway, promotes endothelial mesenchymal transition, activates coagulation pathways, and promotes protein N-homocysteination and cellular hypomethylation, all of which can cause endothelial dysfunction. This article reviews the specific links between HHcy and endothelial dysfunction, and highlights recent evidence that endothelial mesenchymal transition contributes to HHcy-induced vascular damage, with a hope to provide new ideas for the clinical treatment of HHcy-related vascular diseases.
Humans ; Atherosclerosis ; Cardiovascular Diseases ; Endothelium, Vascular ; Homocysteine/metabolism* ; Hyperhomocysteinemia/complications* ; Oxidative Stress ; Risk Factors