Role of Hyperhomocysteinemia and Hyperuricemia in Pathogenesis of Atherosclerosis
| Autor: | Jiangjun Chen, Ning Liu, Hailin Chen, Kui Yang, Youquan Gu, Junjie Zhao, Jun Chen |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Hyperhomocysteinemia Vascular smooth muscle Homocysteine Inflammation Hyperuricemia Nitric Oxide Muscle Smooth Vascular Pathogenesis 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Risk Factors Internal medicine medicine Animals Humans Endothelial dysfunction Cell Proliferation business.industry Rehabilitation medicine.disease Atherosclerosis Endoplasmic Reticulum Stress Uric Acid Endothelial stem cell Oxidative Stress 030104 developmental biology Endocrinology chemistry Surgery Neurology (clinical) Endothelium Vascular medicine.symptom Inflammation Mediators Cardiology and Cardiovascular Medicine business 030217 neurology & neurosurgery Biomarkers Lipoprotein |
| Zdroj: | Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association. 26(12) |
| ISSN: | 1532-8511 |
| Popis: | Background The mechanisms of hyperhomocysteinemia (HHcy) and hyperuricemia (HUA) that promote atherosclerosis were seldom explored and always indefinite. Therefore, we will discuss some new reviews about the role of HHcy and HUA in the pathogenesis of atherosclerosis. Methods This study was conducted by reading a lot of literature, including basic research and clinical application research. Results HHcy is known as an independent risk factor for atherosclerosis. Possible mechanisms for the association between homocysteine and atherosclerosis include stimulating smooth muscle cell growth, reducing endothelial cell growth and endothelial cell relaxation, and decreasing synthesis of high-density lipoprotein. HUA causes endothelial dysfunction and thereby increases oxidative stress, inducing vascular smooth muscle cell proliferation and reducing endothelial nitric oxide bioavailability. HUA plays a role in the development and pathogenesis of metabolic syndrome, hypertension, stroke, and atherosclerosis. Conclusions Accelerated atherosclerosis may be a consequence of the combined effect of HHcy and HUA. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect