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) 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

Atherosclerosis is a chronic inflammatory disease of vascular walls with a complex etiology. In recent years, the incidence of atherosclerosis continues to increase with obesity and diabetes as major risk factors. As an important metabolic organ in the body, adipose tissue also has a powerful endocrine function. In the case of obesity and diabetes, various cytokines and exosomes derived from adipose tissue mediate organ-organ/cell-cell crosstalk, and are involved in the occurrence and development of various diseases. As an important intercellular communicator, exosomes regulate the pathological process of various cardiovascular diseases and are closely related to atherosclerosis. In this paper, we reviewed the mechanism of adipose-derived exosomes in atherosclerosis with focus on endothelial dysfunction, inflammatory response, lipid metabolism disorder and insulin resistance, hoping to provide reference for the research, diagnosis and treatment of atherosclerosis.
Humans ; Exosomes/metabolism* ; Atherosclerosis ; Obesity/complications* ; Adipose Tissue/metabolism* ; Insulin Resistance

Atherosclerosis ; Diabetes Mellitus, Type 2/complications* ; Dyslipidemias ; Fibroblast Growth Factors ; Humans

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

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