Gene polymorphisms associated with non-alcoholic fatty liver disease and coronary artery disease: a concise review. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Li, Xiao-Lin; Sui, Jian-Qing; Lu, Lin-Lin; Zhang, Nan-Nan; Xu, Xin; Dong, Quan-Yong; Xin, Yong-Ning; Xuan, Shi-Ying
• Is Part Of: Lipids in health and disease. Volume 15:Issue 1(2016)
• Page Start: 1
• Page End: 8
• Publication Date: 2016-12
• Subjects: Non-alcoholic fatty liver disease -- Coronary artery disease -- Gene pathogenesis -- Genetic polymorphisms; Lipids -- Periodicals; Lipids in human nutrition -- Periodicals; Lipids -- Metabolism -- Disorders -- Periodicals; 616.3997
• DOI: 10.1186/s12944-016-0221-8
• Languages: English
• ISSNs: 1476-511X

Abstract

Abstract Non-alcoholic fatty liver disease (NAFLD) is a common chronic liver disease which represents a wide spectrum of hepatic damage. Several studies have reported that NAFLD is a strong independent risk factor for coronary artery disease (CAD). And patients with NAFLD are at higher risk and suggested undergoperiodic cardiovascular risk assessment. Cardiovascular disease (CVD) is responsible for the main cause of death in patients with NAFLD, and is mostly influenced by genetic factors. Both NAFLD and CAD are heterogeneous disease. Common pathways involved in the pathogenesis of NAFLD and CAD includes insulin resistance (IR), atherogenic dyslipidemia, subclinical inflammation, oxidative stress, etc . Genomic characteristics of these two diseases have been widely studied, further research about the association of these two diseases draws attention. The gene polymorphisms of adiponectin-encoding gene (ADIPOQ ), leptin receptor (LEPR ), apolipoprotein C3 (APOC3 ), peroxisome proliferator-activated receptors (PPAR ), sterol regulatory elementbinding proteins (SREBP ), transmembrane 6 superfamily member 2 (TM6SF2 ), microsomal triglyceride transfer protein (MTTP ), tumor necrosis factors-alpha (TNF-α ) and manganese superoxide dismutase (MnSOD ) have been reported to be related to NAFLD and CAD. In this review, we aimed to provide an overview of recent insights into the genetic basis of NAFLD and CAD.