Background: The present study aimed to investigate the relationship of non-alcoholic fatty liver disease (NAFLD) with the severity and extent of coronary stenotic lesions calculated by the Gensini score. In addition, the ability of Fibrosis-4 (FIB4) score to differentiate coronary artery calcification (CAC) and its severity is assessed. Methods: The current retrospective study was performed on a total of 342 patients examined between January and December 2016 in an affiliated hospital of Jiaxing University, Zhejiang, China. The study used liver ultrasonography for the assessment of NAFLD. Furthermore, the FIB4 and Gensini scores were used to predict hepatic fibrosis risk and the severity of coronary stenotic lesions. Results: The present study revealed that the serum levels of triglycerides, fasting glucose, alanine aminotransferase, and uric acid were significantly higher in patients with NAFLD than in participants without NAFLD (P < 0.001, P < 0.001, P = 0.032, and P = 0.002). Moreover, cases with NAFLD had a higher percentage of diabetes mellitus and hypertension (P < 0.001 and 0.001) than those without NAFLD. It was noted that the level of high-density lipoprotein was lower in patients with NAFLD than in participants without NAFLD (P = 0.006). In addition, we observed that the Gensini score was higher in patients with NAFLD than in participants without NAFLD (P = 0.033). It was found that 27.3%, 25.8%, 45.7%, and 56.3% of the participants had NAFLD in control, single, double, and multi lesion groups, respectively, and the difference was statistically significant (P = 0.008). The number of diseased vessels in patients with severe NAFLD was higher than in the control group (P < 0.001). It was also evident that the number of affected vessels significantly increased (P = 0.010 and P = 0.001) with the stages of NAFLD predicted by the FIB4 and Gensini scores. Furthermore, the Gensini score in patients with moderate and severe NAFLD was higher than in the control group (P = 0.013 and P = 0.019). We also conducted univariate logistic regression analyses to examine the relationship of CAC with FIB4 scores, and it was not significant (P = 0.191). Conclusions: The present study showed a positive relationship between NAFLD severity and coronary stenotic lesions in the eastern Chinese population. Furthermore, it was found that the higher the degree of FIB4 score, the higher the risk of CAC in patients with NAFLD. Therefore, assessing NAFLD severity using the FIB4 score may be useful for differentiating the patients at a higher risk of CAC. However, further prospective studies are required to establish the link between the FIB4 score and CAC.

Background: Hepatic stellate cells (HSCs) are liver-specific pericytes that transform into myofibroblasts, which are involved in pathological vascularization in liver fibrosis. We previously suggested that A20 overexpression suppresses lipopolysaccharide (LPS)-induced inflammation in HSC. We aimed to determine the mechanisms of the anti-inflammatory role of A20 in LX-2 cells. Methods: LX-2 cells were transfected with A20-siRNA or control-siRNA and control adenovirus or A20-carrying adenovirus. Quantitative reverse transcription PCR (RT-qPCR) analysis was employed to quantify mRNA levels of α-SMA, col-I, col-III, IL-6, TGF-β, and PDGF in A20-siRNA LX-2 cells stimulated with LPS. Multiple molecular indices of MAPK/ERK/JNK signal pathway were performed by using gene transfection and Western blotting. Results: Relative to control, the fibrosis-related mRNA levels of α-SMA, col-I, and col-III were increased in A20-siRNA LX-2 cells. Meanwhile, A20-siRNA cells significantly increased IL-6, TGF-β, and PDGF mRNA levels. Relative to controls, stimulating A20 overexpressing LX-2 cells with LPS for 5 and 30 minutes significantly reduced the levels of phosphorylated ERK and JNK, respectively. A20 knockdown in LX-2 cells promotes phosphorylated ERK and JNK levels with LPS for 30 minutes. Conclusions: Our data indicate that A20 could be functional in HSCs through the MAPK/ERK/JNK signaling pathway, highlighting a potential novel therapeutic strategy against liver fibrosis.