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Dysbiosis of the gastric microbiome is involved in the development of gastric cancer (GC). A number of studies have demonstrated an increase in the relative abundance of Lactobacillus in GC. In this review, we present data that support the overgrowth of Lactobacillus in GC from studies on molecular and bacterial culture of the gastric microbiome, discuss the heterogenic effects of Lactobacillus on the health of human stomach, and explore the potential roles of the overgrowth of Lactobacillus in gastric carcinogenesis. Further studies are required to examine the association between Lactobacillus and GC at strain and species levels, which would facilitate to elucidate its role in the carcinogenic process.

In this paper, poly(lactic acid) (PLA) micro- and nanofibers were successfully prepared by centrifugal spinning which is a more simple and effective approach to produce micro/nanofibers. The morphology of fibers was investigated using scanning electron microscopy (SEM), X-ray diffraction (XRD), while their thermal properties by differential scanning calorimeter (DSC) and thermal gravimetric analysis (TGA). The results showed that the diameter of PLA fibers increased significantly with increasing solution concentration and decreased slightly with increasing collection distance. It can be controlled below 500 nm at the optimal process parameters which were found to be spinning solution concentration of 6 %, spinneret diameter of 0.11 mm, rotational speed of 5500 rpm and collecting distance of 15 cm. Although the crystallinity of the PLA fibers was weaker than that of the PLA pellets due to the insufficient adjustment of the molecular chain in rapid solvent evaporation and short stretching time, it can be improved by increasing the rotational speed from 4500 to 7000 rpm. The glass transition temperature (Tg) and melting temperature (Tm) of the fibers were nearly keeping constant compared to the PLA pellets. Its good degradability was demonstrated by the loss of fibers structure completely within 5 hours of immersion in NaOH at pH 13.

Oncogenic KRAS is considered a promising target for anti-cancer therapy. However, direct pharmacological strategies targeting KRAS-driven cancers remained unavailable. The prenyl-binding protein PDEδ, a transporter of KRAS, has been identified as a potential target for pharmacological inhibitor by selectively binding to its prenyl-binding pocket, impairing oncogenic KRAS signaling pathway. Here, we discovered a novel PDEδ inhibitor (E)-N'-((3-(tert-butyl)-2-hydroxy-6,7,8,9-tetrahydrodibenzo[b,dfuran-1-yl)methylene)-2,4-dihydroxybenzohydrazide(NHTD) by using a high-throughput docking-based virtual screening approach. In vitro and in vivo studies demonstrated that NHTD suppressed proliferation, induced apoptosis and inhibited oncogenic K-RAS signaling pathways by disrupting KRAS-PDEδ interaction in nonsmall cell lung cancer (NSCLC) harboring KRAS mutations. NHTD redistributed the localization of KRAS to endomembranes by targeting the prenyl-binding pocket of PDEδ and exhibited the suppression of abnormal KRAS function. Importantly, NHTD prevented tumor growth in xenograft and KRAS mutant mouse model, which presents an effective strategy targeting KRAS-driven cancer.

Asia, Europe, and Africa, connected by the maritime silk road (MSR) and the land silk road (LSR), as the cradle of ancient civilizations, contain rich cultural heritage resources. While aiming to achieve differentiated and targeted application, protection, and development of world cultural heritage (WCHS), it is essential to identify the temporal-spatial distribution features of WCHS on these three continents. For these WCHS elements, based on big earth data, we semi-quantitatively describe the features of spatial-temporal distribution, material types, civilization and religion characters, capital investment capacity, and risks by data cleaning, spatial analysis, and risk assessment. Our findings reveal features in these WCHS elements, including temporal and spatial distribution, the amount of different ancient civilizations and cultural diversity, and the need for preservation and funding capacity. Finally, this study’s results indicate that we should take full advantage of the potential of cultural heritage, digital technologies, and the scientific protection of cultural heritage along with the MSR and LSR. Moreover, declarations of heritage in Africa and Central Asia should be extended to realize the precise “poverty alleviation” of WCHS protection in these regions. For further planning of WCHS sites along the Silk Road, we propose countermeasures to protect the global cultural heritage in the future and also provide theoretical guidance and specific scientific implementation directions to “strengthen efforts to protect and safeguard the world’s cultural and natural heritage,” as proposed by the United Nations.

A novel type of core-shell "loading-type" nanomaterials, which integrated excellent biocompatibility, high loading capacity, efficient delivery, dual target recognition and response all-in-one, was fabricated for simultaneous imaging analysis of glutathione and microRNAs in living cells. Specifically, the core-shell "loading-type" nanomaterials (termed as MSNs@MnO

Several studies have reported that apolipoprotein A5 (APOA5) is involved in the development of non-alcoholic fatty liver disease (NAFLD). However, no research has been performed regarding the association between APOA5 polymorphisms and the risk of NAFLD. This study aimed to explore the association between APOA5 gene polymorphisms and NAFLD in a Chinese Han population.Genotypes of the SNPs (rs10750097, rs1263173, rs17120035, rs3135507 and rs662799) of APOA5 in 232 NAFLD patients and 188 healthy controls were determined using polymerase chain reaction (PCR) analysis. Clinical characteristics were measured using biochemical methods.The five single nucleotide polymorphisms (SNPs) (rs10750097, rs1263173, rs17120035, rs3135507 and rs662799) of APOA5 showed no significant association with NAFLD (P 0.05). The rs10750097 with G allele showed a higher serum level of alkaline phosphatase (ALP) compared with C allele in overall series and NAFLD patients (P 0.05). The rs1263173(A/A) carriers showed a higher level of glucose compared to the non-carriers in overall series (P 0.05). The rs17120035(T/T) carriers showed a lower plasma TG level in overall series and NAFLD patients (P 0.05), and the rs662799(G/G) carriers showed higher levels of plasma triglyceride (TG), ALP, and lower level of high-density lipoprotein (HDL) compared to non-carriers in NAFLD patients (P 0.05). No significant difference were observed on the clinic parameters of APOA5 rs3135507(T/T) carriers in both group of overall series and NAFLD patients (P 0.05).The five SNPs (rs10750097, rs1263173, rs17120035, rs3135507 and rs662799) of APOA5 gene are not associated with the risk of NAFLD in the Chinese Han population. The genotypes of rs10750097(G/G), rs1263173(A/A), rs17120035(T/T), and rs662799(G/G) performed a significant effect on clinic characteristics in overall series and NAFLD patients, indicating that these polymorphisms may be associated with NAFLD.

World heritage is a precious treasure left to mankind by history. It is a treasure of all human civilization and has very important historical, artistic and scientific value. Protecting world cultural heritage is a prerequisite for protecting the inheritance of human culture, safeguarding the diversity and creativity of the world’s culture, and promoting the development of mankind. However, the rapid urbanization process globally has changed the land cover/land use, transportation and environmental conditions in cities, and has caused some impacts and damages to the world heritage sites. Based on three global Earth Observation datasets including Global Human Settlement Layer (GHSL), global population grid products (Worldpop) and the global night-time light images (DMSP/OLS), this paper proposed an urbanization intensity index (UII) to dynamically monitor and quantitatively assess the intensity of urbanization around the world heritage sites. Large UII values represent high urbanization degrees in the study area, and vice versa. The rapid increase of UII indicated that great impacts might be caused by the urban development process on corresponding heritage sites. The assessment results showed that the mean value of UII at 10 world cultural heritage sites in China’s urban areas increased from 0.35 in 2000 to 0.42 in 2015. The urbanization intensity index of the world cultural heritage sites can provide valuable datasets and scientific basis for the protection and development of world cultural heritage sites.

Deltarasin is a recently identified small molecule that can inhibit KRAS–PDEδ interactions by binding to a hydrophobic pocket on PDEδ, resulting in the impairment of cell growth, KRAS activity, and RAS/RAF signaling in human pancreatic ductal adenocarcinoma cell lines. Since KRAS mutations are the most common oncogene mutations in lung adenocarcinomas, implicated in over 30% of all lung cancer cases, we examined the ability of deltarasin to inhibit KRAS-dependent lung cancer cell growth. Here, for the first time, we document that deltarasin produces both apoptosis and autophagy in KRAS-dependent lung cancer cells in vitro and inhibits lung tumor growth in vivo. Deltarasin induces apoptosis by inhibiting the interaction of with PDEδ and its downstream signaling pathways, while it induces autophagy through the AMPK-mTOR signaling pathway. Importantly, the autophagy inhibitor, 3-methyl adenine (3-MA) markedly enhances deltarasin-induced apoptosis via elevation of reactive oxygen species (ROS). In contrast, inhibition of ROS by N-acetylcysteine (NAC) significantly attenuated deltarasin-induced cell death. Collectively, these observations suggest that the anti-cancer cell activity of deltarasin can be enhanced by simultaneously blocking “tumor protective” autophagy, but inhibited if combined with an anti-oxidant.

// Ying-Min Wu 1, * , Zhuo-Jia Chen 2, * , Hao Liu 3 , Wei-Dong Wei 2 , Lin-Lin Lu 1 , Xiang-Ling Yang 4, 5 , Wei-Ting Liang 2 , Tao Liu 2 , Huan-Liang Liu 4, 5 , Jun Du 1 , Hong-Sheng Wang 1 1 Department of Microbial and Biochemical Pharmacy, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China 2 Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China 3 Cancer Research Institute and Cancer Hospital, Guangzhou Medical University, Guangzhou 510095, China 4 Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, Guangdong Institute of Gastroenterology and The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou 510655, China 5 Institute of Human Virology and Key Laboratory of Tropical Disease Control of Ministry of Education, Sun Yat-sen University, Guangzhou 510080, China * These authors have contributed equally to this work Correspondence to: Hong-Sheng Wang, e-mail: whongsh@mail.sysu.edu.cn , hongshengwang@foxmail.com Jun Du, e-mail: dujun@mail.sysu.edu.cn Keywords: ERRα, TNBC, EMT, fibronectin Received: April 15, 2015 Accepted: June 16, 2015 Published: June 26, 2015 ABSTRACT Triple-negative breast cancer (TNBC) patients have poor prognosis due to the aggressive metastatic behaviors. Our study reveals that expression of estrogen related receptor α (ERRα) is significantly ( p < 0.01) positively associated with high grade tumors and lymph node metastasis, while negatively correlated with overall survival (OS), in 138 TNBC patients. Targeted inhibition of ERRα by its inverse agonist XCT-790 or si-RNA obviously inhibits in vitro motility of TNBC cells. While over expression of ERRα triggers the invasion and migration of TNBC cells. Further, si-ERRα and XCT-790 inhibit the epithelial mesenchymal transition (EMT) of TNBC cells with increasing the expression of E-cadherin and decreasing fibronectin (FN) and vimentin. While XCT-790 has no effect on the expression of EMT related transcription factors such as Snail or Slug. Further, inhibitors of MAPK, PI3K/Akt, NF-κB signal molecules, which are activated by XCT-790, can not attenuate the suppression effects of XCT-790 on EMT. Alternatively, luciferase reporter gene assays and ChIP analysis indicate that ERRα can directly bind with FN promoter at ERR response element-3 (ERRE-1), ERRE-3, and ERRE-4, while XCT-790 reduces this bond. In vivo data show that ERRα expression is significantly ( p < 0.05) correlated with FN in clinical TNBC patients. In MDA-MB-231 tumor xenograft models, XCT-790 decreases the expression of FN, inhibits the growth and lung metastasis, and suppresses the EMT. Our results demonstrate that ERRα functions as a metastasis stimulator and its targeted inhibition may be a new therapeutic strategy for TNBC treatment.

Systemic diseases often have common characteristics. The aim of this study was to investigate the feasibility of targeting common pathological metabolism to inhibit the progression of malignant and proliferative diseases.Gefitinib-resistant (G-R) nonsmall-cell lung cancer (NSCLC) and rheumatoid arthritis (RA) were studied as conditions representative of malignant and proliferative diseases, respectively. Strong lipogenic activity and high expression of sterol regulatory element-binding protein 1 (SREBP1) were found in both G-R NSCLC cells and synovial fibroblasts from RA patients (RASFs). Berberine (BBR), an effective suppressor of SREBP1 and lipogenesis regulated through reactive oxygen species (ROS)/AMPK pathway, selectively inhibited the growth of G-R NSCLC cells and RASFs but not that of normal cells. It effectively caused mitochondrial dysfunction, activated ROS/AMPK pathway, and finally suppressed cellular lipogenesis and cell proliferation. Addition of ROS blocker, AMPK inhibitor, and palmitic acid significantly reduced the effect of BBR. In an in vivo study, treatment of BBR led to significant inhibition of mouse tumor xenograft growth and remarkably slowed down the development of adjuvant-induced arthritis in rats. Innovation and Conclusion: Targeting ROS/AMPK/lipogenesis signaling pathway selectively inhibited the growth of G-R NSCLC cells and the progress of RASFs in vitro and in vivo, which provides a new avenue for treating malignancies and proliferative diseases. Antioxid. Redox Signal. 28, 339-357.

Background A growing number of studies reported the connection between the level of serum ferritin (SFL) and non-alcoholic fatty liver disease (NAFLD). However, such connection was still disputable. The aim of our meta-analysis was to estimate SFL between the groups as below: patients with NAFLD against control group; non-alcoholic steatohepatitis (NASH) patients against control group; non-alcoholic fatty liver (NAFL) patients against a control group and NASH patients vs NAFL patients. Methods We screened the studies in PubMed, EMBASE, the Cochrane Database and the Cochrane Central register controlled trials from the beginning to July 10, 2016 to find the studies indicated the connection between SFL and NAFLD (NAFL and/or NASH). Fourteen published studies which evaluate the SFL in NAFLD patients were selected. Results Higher SFL was noticed in NAFLD patients against control group (standardized mean difference [SMD] 1.01; 95% CI 0.89, 1.13), NASH patients against control group (SMD 1.21; 95% CI 1.00, 1.42), NAFL patients against control group (SMD 0.51; 95% CI 0.24, 0.79) and NASH patients against NAFL patients (SMD 0.63; 95% CI 0.52, 0.75). These results remained unaltered actually after the elimination of studies which were focused on paediatric or adolescent populations. Higher SFL was presented in NAFLD patients against the control group (SMD 1.08; 95% CI 0.95, 1.20) in adults and NASH patients against NAFL patients in adults (SMD 0.74; 95% CI 0.62, 0.87). The connection between SFL and NASH against NAFL group in paediatric or adolescent populations was observed inconsistently (SMD 0.10; 95% CI -0.18, 0.38). Conclusions The level of SFL was elevated in patients with NAFLD (NAFL and/or NASH) compared with the controls. Compared with NAFL, The level of SFL was increased in NASH. The result remained unaltered actually after the elimination of studies focused on paediatric or adolescent populations.

Background Some studties reported that the polymorphism of TM6SF2 gene E167K affects the occurrence and the progression of hepatocytes carcinoma (hepatocellular, HCC). In oeder to investigate the effects of the polymorphism of TM6SF2 gene E167K in the pathogenesis of HCC, we explored its influence on the cell cycle in hepatocellular carcinoma cell HEPA1-6. Methods HEPA 1–6 cells which could respectively overexpress TM6SF2 wild type and E167K variant were cultured and HEPA 1–6 cells with zero load plasmids were used as matched control. Flow cytometry was used to detect the cell cycles of these 3 type of HEPA 1–6 cells. Realtime fluores-cence quantitative PCR and western blot were used to analyzed the expression of regulatory factors (Cyclin D1、p53、P16、P27、P21 and Rb) of cell cycle. T-test was used in statistical analysis. Results Cell cycle phase distribution was presented by the proportion of cells in each phases (%). Compared with the control group, the cell cycle phase distribution (G1 phase 57.36 ± 0.21%, G2/M phase 25.61 ± 0.36%,S phases 19.31 ± 0.25%) had no differences in wild type group (G1 phase 57.63 ± 0.28%, G2/M phase 25.77 ± 0.51%, S phases 19.54 ± 0.25%; P 0.05). P16 and P21 expression showed no statistical sigtfificance in any of these three groups (P > 0.05). Conclusion E167K polymorphism of TM6SF2 gene affects cell cycles of HEPA1–6 cells via up-regulating CyclinD1、P53 and Rb and down-regulating P27.

Aconitum, widely used to treat rheumatoid arthritis for thousands of years, is a toxic herb that can frequently cause fatal cardiac poisoning.Aconitumtoxicity could be decreased by properly hydrolyzing diester-diterpene alkaloids into monoester-diterpene alkaloids. Monoester-diterpene alkaloids, including benzoylaconine (BAC), benzoylmesaconine (BMA), and benzoylhypaconine (BHA), are the primary active and toxic constituents of processedAconitum. Cytochrome P450 (CYP) enzymes protect the human body by functioning as the defense line that limits the invasion of toxicants. Our purposes were to identify the CYP metabolites of BAC, BMA, and BHA in human liver microsomes and to distinguish which isozymes are responsible for their metabolism through the use of chemical inhibitors, monoclonal antibodies, and cDNA-expressed CYP enzyme. High-resolution mass spectrometry was used to characterize the metabolites. A total of 7, 8, and 9 metabolites were detected for BAC, BMA, and BHA, respectively. The main metabolic pathways were demethylation, dehydrogenation, demethylation-dehydrogenation, hydroxylation and didemethylation, which produced less toxic metabolites by decomposing the group responsible for the toxicity of the parent compound. Taken together, the results of the chemical inhibitors, monoclonal antibodies, and cDNA-expressed CYP enzymes experiments demonstrated that CYP3A4 and CYP3A5 have essential functions in the metabolism of BAC, BMA, and BHA.

Background Cardiovascular disease (CAD) responsible and nonalcoholic fatty liver disease (NAFLD) are both metabolic diseases, and they are mostly influenced by genetic factors. The aim of our study is to evaluate the relationship between angiotensin II type-1 receptor (AGTR1) gene rs3772622 polymorphisms and the risk of developing coronary artery disease (CAD) in Chinese patients with NAFLD. Methods Genotype for AGTR1 rs3772622 in 574 NAFLD patients with CAD or 589 NAFLD patients without CAD, 332 CAD patients exclude NAFLD and 338 health control subjects were determined by sequencing and polymerase chain reaction analysis. Relevant statistical methods were employed to analyze the genotypes, alleles and the clinical date. Inter-group differences and associations were assessed statistically using t-tests and Chi square and logistic analyses. The relative risk of AGTR1 rs3772622 for NAFLD was estimated by logistic regression analysis. Results No significant difference in genotype and allele frequency of AGTR1 rs3772622 was found between the NAFLD without CAD population and the controls (P > 0.05). However, makeable difference was found when compared the CAD in patients with NAFLD and CAD free NAFLD patients (P

In this paper, a job shop scheduling model combining MAS (Multi-Agent System) with GASA (Simulated Annealing-Genetic Algorithm) is presented. The proposed model is based on the E2GPGP (extended extended generalized partial global planning) mechanism and utilizes the advantages of static intelligence algorithms with dynamic MAS. A scheduling process from ‘initialized macro-scheduling’ to ‘repeated micro-scheduling’ is designed for large-scale complex problems to enable to implement an effective and widely applicable prototype system for the job shop scheduling problem (JSSP). Under a set of theoretic strategies in the GPGP which is summarized in detail, E2GPGP is also proposed further. The GPGP-cooperation-mechanism is simulated by using simulation software DECAF for the JSSP. The results show that the proposed model based on the E2GPGP-GASA not only improves the effectiveness, but also reduces the resource cost.

The time series ARIMA (3,1,4) model was established, which is taken into use of price forecasting. Then the forecasted price was applied to mining technical and economic index optimization study. Lead prices could be reliably predicted by time series ARIMA model, which had a high accuracy and the percentage of prediction error was 2.97% on average. It can solve the problems of the price data lag in the study of mine economic index optimization very well.

Based on system modeling, including ore reserves model, mineral processing model and comprehensive technical economic analysis model, the major economic indexes of Cangshang Gold Mine were multi-objective optimized by fuzzy comprehensive evaluation. After optimization, the total profits, gold output and NPV were improved.

Nonalcoholic fatty liver disease (NAFLD) is a metabolic stress-induced liver disease that is closely related not only to genetic susceptibility but also to insulin resistance and highly linked with metabolic syndrome. In recent years, the prevalence of NAFLD has increased rapidly, paralleling the epidemic of type 2 diabetes mellitus and obesity leading to cardiovascular disease. It has been demonstrated that NAFLD is highly associated with atherosclerosis. With recently gained knowledge, it appears that NAFLD may induce insulin resistance, dyslipidemia, oxidative stress, inflammation, and fluctuation of adipokines associated with atherosclerosis. In this review, we aimed to summarize recent discoveries related to both NAFLD and atherosclerosis, and to identify possible mechanisms linking them.

Ti3SiC2/SiC composites were fabricated by reactive hot pressing method. Effect of processing condition on the microstructure and mechanical properties of the composites were investigated. The results showed that: (1) Hot-pressing temperature influenced the phase constituent of Ti3SiC2/SiC composites. The flexural strength and fracture toughness of composites increased with hot pressing temperature. (2) The flexural strength and fracture toughness of composites increased when the content of SiC was increased. When the SiC content was 30wt% the flexural strength and fracture toughness of Ti3SiC2/SiC composite were 371MPa and 6.9MPa•m1/2 respectively. However, when the content of SiC reached 50wt%, the flexural strength and fracture toughness of composites decreased due to high porosity in the composites. (3) The flexural strength and fracture toughness of composites increased with the particle size of SiC added in composites. (4) Ti3SiC2/SiC composites were non-brittle at room temperature.

Rhein, a lipophilic anthraquinone, exhibits anti-inflammatory and anti-tumor activities; however, it is hepatotoxic. ATP-binding cassette transporters, including P-glycoprotein (P-gp), breast cancer resistance protein (BCRP) and multidrug resistance-associated protein 2 (MRP2), can pump toxicants from gut epithelial cells back into the intestinal lumen to prevent poisoning. We investigated their roles in rhein transport using a rat intestinal perfusion model and Caco-2, MDCKII-MDR1 (high expression of P-gp), MDCKII-BCRP (high expression of BCRP) and MDCKII-MRP2 (high expression of MRP2) cell models. The permeability of rhein in the duodenum significantly increased with increasing perfused concentration of rhein in the rat model, suggesting that efflux transporters were involved in rhein transport. In the Caco-2 cells, the permeability of rhein from the basolateral (B) to the apical (A) was significantly higher than that from A to B. In the presence of BCRP or MRP2 inhibitor, the permeability of rhein significantly decreased from B to A direction. In the MDCKII-BCRP cells, rhein was more permeable in B to A side than that in the opposite side. However, no significant differences of rhein permeability were observed in two directions in both MDCKII-MDR1 and MDCKII-MRP2 cells. Taken together, these results suggested that only BCRP was involved in rhein transport.

Geological section can help validating and understanding of the alteration information which is extracted from remote sensing images. In the paper, the concept of spectral geological profile was introduced based on the principle of geological section and the method of spectral information extraction. The spectral profile can realize the storage and vision of spectra along the geological profile, but the spectral geological spectral profile includes more information besides the information of spectral profile. The main object of spectral geological spectral profile is to obtain the distribution of alteration types and content of minerals along the profile which can be extracted from spectra measured by field spectrometer, especially for the spatial distribution and mode of alteration association. Technical method and work flow of alteration information extraction was studied for the spectral geological profile. The spectral geological profile was set up using the ground reflectance spectra and the alteration information was extracted from the remote sensing image with the help of typical spectra geological profile. At last the meaning and effect of the spectral geological profile was discussed.

Background Recently genome-wide association studies identified that NCAN rs2228603 polymorphism was associated with non-alcoholic fatty liver disease (NAFLD) mainly in subjects of European ancestry. While no research have been conducted to demonstrate the relationship between NCAN rs2228603 and NAFLD in Chinese Han adults. The aim of this study was to investigate whether NCAN rs2228603 is associated with NAFLD in Chinese population. Methods Gene NCAN rs2228603 was genotyped in 182 patients with NAFLD and 195 healthy controls. The expression of NCAN was tested according to polymerase chain reaction analysis (PCR) and serum lipids were performed by biology techniques. Results No significant difference was found in genotype and allele frequencies of NCAN rs2228603 between the NAFLD group and the controls (P > 0.05). Subjects with the NCAN rs2228603 CT genotype showed a higher level of alkaline phosphatase (AKP) (P = 0.017) and a higher high-density lipoprotein (HDL) (P

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.