HSPA8 Single-Nucleotide Polymorphism Is Associated with Serum HSC70 Concentration and Carotid Artery Atherosclerosis in Nonalcoholic Fatty Liver Disease

Abstract

There is an association between nonalcoholic fatty liver disease (NAFLD) and atherosclerosis, but the genetic risk of atherosclerosis in NAFLD remains unclear. Here, a single-nucleotide polymorphism (SNP) of the heat shock 70 kDa protein 8 (HSPA8) gene was analyzed in 123 NAFLD patients who had been diagnosed using a liver biopsy, and the NAFLD phenotype including the maximum intima–media thickness (Max-IMT) of the carotid artery was investigated. Patients with the minor allele (A/G or G/G) of rs2236659 showed a lower serum heat shock cognate 71 kDa protein concentration than those with the major A/A allele. Compared with the patients with the major allele, those with the minor allele showed a higher prevalence of hypertension and higher Max-IMT in men. No significant associations between the HSPA8 genotype and hepatic pathological findings were identified. In decision-tree analysis, age, sex, liver fibrosis, and HSPA8 genotype were individually associated with severe carotid artery atherosclerosis (Max-IMT ≥ 1.5 mm). Noncirrhotic men aged ≥ 65 years were most significantly affected by the minor allele of HSPA8. To predict the risk of atherosclerosis and cardiovascular disease, HSPA8 SNP genotyping might be useful, particularly for older male NAFLD patients.

Identification of Key Genes and Underlying Mechanisms in Cystic Fibrosis and its Associated Complications Based on Bioinformatics Analysis of Next Generation Sequencing Data Analysis

“…Accumulating evidence shows that MMP9 [133], S100A12 [148], HP (haptoglobin) [149], OSM (oncostatin M) [150], PRDM5 [151], TSPO (translocator protein) [152], IL18RAP [153], ADAMDEC1 [154], IL1RN [155], SCN9A [156], FADS2 [157], NCF4 [158], SERPINB1 [159], TNFRSF13B [160], IL2RB [161], DLG5 [162], FASLG (Fas ligand) [163], GPR68 [164], IL2RA [161], TCF4 [165], TAGAP (T cell activation RhoGTPase activating protein) [166], ABCB1 [167], FCRL3 [168], ITGB7 [169], PTGER4 [170] and TRAF3IP2 [171] are altered expression in gastrointestinal complications. Recent studies reported that MMP9 [133], S100A12 [172], IGF2 [173], GPR84 [174], SOCS3 [175], IGFBP2 [176], HP (haptoglobin) [177], MMP8 [178], OSM (oncostatin M) [179], TLR5 [180], S100A9 [181], PLIN5 [182], NRG1 [183], LCN2 [184], TSPO (translocator protein) [185], PLAU (plasminogen activator, urokinase) [186], PPBP (pro-platelet basic protein) [187], UPP1 [188], ALOX5 [189], IL1RN [190], CYP1B1 [191], DGAT2 [192], MSRA (methionine sulfoxidereductase A) [193], ADAM9 [194], CPEB4 [195], IRS2 [196], FADS2 [197], SLC22A4 [198], PFKFB3 [199], CTSD (cathepsin D) [200], ADAM12 [201], CD80 [202], ERBB2 [203], FASLG (Fas ligand) [204], CNR2 [205], SOCS2 [206], ABCB1 [207], CD74 [208], FCRL3 [209], PARP1 [210], TXNIP (thioredoxin interacting protein) [211], TULP3 [212], HSPA8 [213], TNIK (TRAF2 and NCK interacting kinase) [214], PDCD4 [215…”