Endothelial dysfunction in nonalcoholic fatty liver disease

Angela Peltec, Murad Alnabghalie
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Abstract

Introduction. The prevalence of nonalcoholic fatty liver disease (NAFLD) in western countries is increasing rapidly and is considered as component of metabolic syndrome. Endothelial dysfunction is a pathophysiological problem of cardiovascular disease. NAFLD, as a component of metabolic syndrome, is associated with endothelial dysfunction. Material and methods. PubMed database was used in order to review and select articles according to the keywords. A total of 216 articles matching search criteria were found between 2000-2021. Results. The present study has been underlined the role of pathophysiological mechanisms of endothelial dysfunction in nonalcoholic fatty liver disease, which involves oxidative stress, inflammation and insulin resistance. The main factor in the occurrence of endothelial dysfunction is related to nitric oxide (NO) biosynthesis. The markers associated with regulation of nitric oxide biosynthesis, such as asymmetric dimethylarginine, free fatty acid, lectin-like oxidized low-density lipoprotein (LDL) receptor-1 and pentraxin-3, are potential targets in the assessment of endothelial dysfunction. Conclusions. Insulin resistance, inflammation and oxidative stress have been involved in the reduction of NO biosynthesis that influences the occurrence of endothelial dysfunction. Markers, such as lectin-like oxidized LDL receptor-1 and pentraxin-3, have been considered as potential targets in the assessment of endothelial dysfunctions in NAFLD.
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非酒精性脂肪肝的内皮功能障碍
介绍。非酒精性脂肪性肝病(NAFLD)在西方国家的患病率迅速上升,被认为是代谢综合征的组成部分。内皮功能障碍是心血管疾病的病理生理问题。NAFLD作为代谢综合征的一个组成部分,与内皮功能障碍有关。材料和方法。使用PubMed数据库,根据关键词对文章进行评审和选择。2000年至2021年间,共发现216篇符合搜索标准的文章。结果。本研究强调了内皮功能障碍在非酒精性脂肪性肝病中的病理生理机制,包括氧化应激、炎症和胰岛素抵抗。内皮功能障碍发生的主要因素与一氧化氮(NO)的生物合成有关。与一氧化氮生物合成相关的标志物,如不对称二甲基精氨酸、游离脂肪酸、凝集素样氧化低密度脂蛋白(LDL)受体-1和戊曲辛-3,是评估内皮功能障碍的潜在靶点。结论。胰岛素抵抗、炎症和氧化应激参与了一氧化氮生物合成的减少,从而影响内皮功能障碍的发生。凝集素样氧化LDL受体-1和戊曲霉素-3等标志物被认为是评估NAFLD内皮功能障碍的潜在靶点。
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CiteScore
0.20
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0
审稿时长
10 weeks
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