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Sorbitol is a major photosynthate produced in leaves and transported through the phloem of apple (Malus domestica) and other tree fruits in Rosaceae. Sorbitol stimulates its own metabolism, but the underlying molecular mechanism remains unknown. Here, we show that sucrose nonfermenting 1 (SNF1)-related protein kinase 1 (SnRK1) is involved in regulating the sorbitol-responsive expression of both SORBITOL DEHYDROGENASE 1 (SDH1) and ALDOSE-6-PHOSPHATE REDUCTASE (A6PR), encoding 2 key enzymes in sorbitol metabolism. SnRK1 expression is increased by feeding of exogenous sorbitol but decreased by sucrose. SnRK1 interacts with and phosphorylates the basic leucine zipper (bZIP) transcription factor bZIP39. bZIP39 binds to the promoters of both SDH1 and A6PR and activates their expression. Overexpression of SnRK1 in ‘Royal Gala’ apple increases its protein level and activity, upregulating transcript levels of both SDH1 and A6PR without altering the expression of bZIP39. Of all the sugars tested, sorbitol is the only 1 that stimulates SDH1 and A6PR expression, and this stimulation is blocked by RNA interference (RNAi)-induced repression of either SnRK1 or bZIP39. These findings reveal that sorbitol acts as a signal regulating its own metabolism via SnRK1-mediated phosphorylation of bZIP39, which integrates sorbitol signaling into the SnRK1-mediated sugar signaling network to modulate plant carbohydrate metabolism.

Lower-grade gliomas (LGG), characterized by heterogeneity and invasiveness, originate from the central nervous system. Although studies focusing on molecular subtyping and molecular characteristics have provided novel insights into improving the diagnosis and therapy of LGG, there is an urgent need to identify new molecular subtypes and biomarkers that are promising to improve patient survival outcomes. Here, we proposed a joint similarity network fusion (Joint-SNF) method to integrate different omics data types to construct a fused network using the Joint and Individual Variation Explained (JIVE) technique under the SNF framework. Focusing on the joint network structure, a spectral clustering method was employed to obtain subtypes of patients. Simulation studies show that the proposed Joint-SNF method outperforms the original SNF approach under various simulation scenarios. We further applied the method to a Chinese LGG data set including mRNA expression, DNA methylation and microRNA (miRNA). Three molecular subtypes were identified and showed statistically significant differences in patient survival outcomes. The five-year mortality rates of the three subtypes are 80.8%, 32.1%, and 34.4%, respectively. After adjusting for clinically relevant covariates, the death risk of patients in Cluster 1 was 5.06 times higher than patients in other clusters. The fused network attained by the proposed Joint-SNF method enhances strong similarities, thus greatly improves subtyping performance compared to the original SNF method. The findings in the real application may provide important clues for improving patient survival outcomes and for precision treatment for Chinese LGG patients. An R package to implement the method can be accessed in Github at https://github.com/Sameerer/Joint-SNF.

Flavonoids are important metabolites of pigeon pea in relation to its stress resistance. However, the molecular basis and regulatory mechanisms of flavonoids in pigeon pea remain unclear. Methyl jasmonate (MeJA) is a signaling molecule associated with biosynthesis of flavonoids. In this study, after exogenous treatment of 10 mg/L MeJA, infection of pathogenic fungi to pigeon pea was alleviated and the content of flavonoids was increased. Results of gene expression and metabolic changes that were respectively analyzed by transcriptome sequencing and high performance liquid chromatography (HPLC) showed that (1) concentrations of various flavonoids, such as genistein, apigenin, vitexin and biochanin A were significantly up-regulated; (2) 13675 differentially expressed genes were produced, mainly enriched in signal transduction and isoflavone biosynthesis pathways: (3) the expression levels of key synthase genes (CcI2′H, CcHIDH, Cc7-IOMT) in the flavonoid biosynthesis pathway were significantly up-regulated; (4) Overexpression of CcbHLH35 significantly induced upregulation of flavonoid synthase genes and accumulation of genistein, vitexin and apigenin. Our findings reveals the pivotal roles of MeJA in synthesis and functioning of flavonoids in pigeon pea, which provide a basis for further studies on flavonoid-mediated defense responses.

Calcineurin B-like (CBL)-interacting protein kinases (CIPKs) play a central role in Ca2+ signalling and promote drought tolerance in plants. The CIPK gene family in pigeon pea (Cajanus cajan L.), a major food crop affected by drought, has not previously been characterised. Here, we identified 28 CIPK genes in the pigeon pea genome. Five CcCIPK genes were strongly upregulated in roots upon drought treatment and were selected for further characterisation. Overexpression of CcCIPK13 and CcCIPK14 increased survival rates by two- to three-fold relative to controls after 14 days of drought. Furthermore, the three major flavonoids, genistin, genistein and apigenin, were significantly upregulated in the same transgenic plants. Using CcCIPK14 as bait, we performed a yeast two-hybrid screen and identified six interactors, including CcCBL1. CcCIPK14 exhibited autophosphorylation and phosphorylation of CcCBL1 in vitro. CcCBL1-overexpressed plants displayed higher survival rates upon drought stress as well as higher expression of flavonoid biosynthetic genes and flavonoid content. CcCIPK14-overexpressed plants in which CcCBL1 transcript levels were reduced by RNA interference had lower survival rates, which indicated CcCBL1 in the same pathway as CcCIPK14. Together, our results demonstrate a role for the CcCIPK14-CcCBL1 complex in drought stress tolerance through the regulation of flavonoid biosynthesis in pigeon pea.

Graphical abstract, Heart failure with preserved ejection fraction (HFpEF) is associated with multiple etiologic and pathophysiologic factors. HFpEF leads to significant cardiovascular morbidity and mortality. There are various reasons that fail to identify effective therapeutic interventions for HFpEF, primarily due to its clinical heterogeneity causing significant difficulties in determining physiologic and prognostic implications for this syndrome. Thus, identifying clinical subtypes using multi-omics data has great implications for efficient treatment and prognosis of HFpEF patients. Here we proposed to integrate mRNA, DNA methylation and microRNA (miRNA) expression data of HFpEF with a similarity network fusion (SNF) method following a network enhancement (ne-SNF) denoising technique to form a fused network. A spectral clustering method was then used to obtain clusters of patient subtypes. Experiments on HFpEF datasets demonstrated that ne-SNF significantly outperforms single data subtype analysis and other integrated methods. The identified subgroups were shown to have statistically significant differences in survival. Two HFpEF subtypes were defined: a high-risk group (16.8%) and a low-risk group (83.2%). The 5-year mortality rates were 63.3% and 33.0% for the high- and low-risk group, respectively. After adjusting for the effects of clinical covariates, HFpEF patients in the high-risk group were 2.43 times more likely to die than the low-risk group. A total of 157 differentially expressed (DE) mRNAs, 2199 abnormal methylations and 121 DE miRNAs were identified between two subtypes. They were also enriched in many HFpEF-related biological processes or pathways. The ne-SNF method provides a novel pipeline for subtype identification in integrated analysis of multi-omics data.

Cancer cells use aerobic glycolysis to sustain their proliferation. Long non‑coding RNA brain cytoplasmic RNA 1 (BCYRN1) has been reported to act as an oncogene in non‑small‑cell lung cancer (NSCLC). The present study investigated the role of BCYRN1 in NSCLC glycolysis. BCYRN1 expression was detected in NSCLC cells and tissues using reverse transcription‑quantitative PCR. The effect of BCYRN1 on aerobic glycolysis was examined by measuring NSCLC cell glucose catabolism and lactate synthesis. The relationships between BCYRN1 and microRNA (miR)‑149, and between miR‑149 and pyruvate kinase M1/2 (PKM2) were measured using a dual‑luciferase reporter assay. Cell proliferation and invasion were analyzed by the Cell Counting kit‑8 assay and the Matrigel invasion assay, respectively. High BCYRN1 expression was observed in NSCLC tissues and cells compared with the corresponding controls. BCYRN1 induced glycolysis and upregulated the expression levels of PKM2 in NSCLC cells. In addition, BCYRN1 regulated miR‑149 expression levels, and miR‑149 inhibitor rescued the effects of si‑BCYRN1 on glucose consumption and lactate production. miR‑149 knockdown significantly enhanced the expression of PKM2. Furthermore, PKM2 inhibition significantly reversed the effects of miR‑149 inhibitor on glucose catabolism and lactate synthesis. Furthermore, PKM2 was involved in NSCLC cell proliferation and invasion, and BCYRN1 knockdown and miR‑149 overexpression inhibited both processes. The present study suggested that BCYRN1 was involved in cell glycolysis, proliferation and invasion during NSCLC via regulating miR‑149 and PKM2.

Sugar, acting as a signal, can regulate the production of some chemical substance during plant defense responses. However, the molecular basis and regulatory mechanisms of sugar in poplar and other forest trees are still unclear. Sorbitol is a sugar-signaling molecule associated with plant defense. In this study, the pathogen-infested status of poplar was alleviated after exogenous feeding of 50 mM sorbitol. We sequenced and analyzed the transcriptome of poplar leaves before and after inoculation. The results showed that the genes PR1, WRKY, ceramide kinases (CERK) and so on responded to sorbitol feeding and pathogen infestation. We screened for genes related to disease resistance such as PsWRKY25 and PsCERK1 and found that significant disease spots occurred on day six of strep throat infestation. Under sorbitol feeding conditions, the appearance of spots was delayed after the pathogen inoculation. Due to the overexpression of PsWRKY25, the overexpression of PsCERK1 triggered the defense response in poplar. This was also confirmed by PsWRKY25 overexpression experiments. These findings present new insights into the influence of sorbitol on Populus simonii Carr. disease resistance. These results emphasize the value of molecular phenotypes in predicting physiological changes.

Mature pollen germinates rapidly on the stigma, extending its pollen tube to deliver sperm cells to the ovule for fertilization. The success of this process is an important factor that limits output. The flavonoid content increased significantly during pollen germination and pollen tube growth, which suggests it may play an important role in these processes. However, the specific mechanism of this involvement has been little researched. Our previous research found that hyperoside can prolong the flowering period of Abelmoschus esculentus (okra), but its specific mechanism is still unclear. Therefore, in this study, we focused on the effect of hyperoside in regulating the actin-depolymerizing factor (ADF), which further affects the germination and growth of pollen. We found that hyperoside can prolong the effective pollination period of okra by 2–3-fold and promote the growth of pollen tubes in the style. Then, we used Nicotiana benthamiana cells as a research system and found that hyperoside accelerates the depolymerization of intercellular microfilaments. Hyperoside can promote pollen germination and pollen tube elongation in vitro. Moreover, AeADF1 was identified out of all AeADF genes as being highly expressed in pollen tubes in response to hyperoside. In addition, hyperoside promoted AeADF1-mediated microfilament dissipation according to microfilament severing experiments in vitro. In the pollen tube, the gene expression of AeADF1 was reduced to 1/5 by oligonucleotide transfection. The decrease in the expression level of AeADF1 partially reduced the promoting effect of hyperoside on pollen germination and pollen tube growth. This research provides new research directions for flavonoids in reproductive development.

Cerebral ischemia/reperfusion (I/R) injury leads to neuronal damage, which may cause disability and even mortality. Multiple studies have revealed that long non‑coding RNAs (lncRNAs) serve pivotal roles in the pathogenesis of cerebral I/R injury. Therefore, the present study aimed to investigate whether the lncRNA X inactivate‑specific transcript (XIST) protects neuronal cells from cerebral I/R injury. In the present study, reverse transcription‑quantitative PCR demonstrated that XIST expression was upregulated in the brain tissues of an I/R mouse model and in oxygen and glucose deprivation/reperfusion (OGD/R)‑treated Neuro‑2a (N2a) cells. Knockdown of XIST alleviated cerebral injury, as well as reduced N2a cell apoptosis and reactive oxygen species (ROS) production. Additionally, luciferase reporter and RNA immunoprecipitation assays identified that XIST could bind with microRNA (miR)‑27a‑3p. It was found that miR‑27a‑3p expression was downregulated in the brain tissues of an I/R mouse model and in OGD/R‑induced N2a cells. In addition, miR‑27a‑3p overexpression attenuated I/R‑induced cerebral injury, and inhibited the apoptosis and ROS production of N2a cells. miR‑27a‑3p was found to target FOXO3. Silencing of FOXO3 alleviated cerebral injury, as well as inhibited N2a cell apoptosis and ROS production. Collectively, these findings indicated that XIST aggravated cerebral I/R injury by regulating miR‑27a‑3p/FOXO3 signaling, which may provide a novel insight into the treatment of cerebral I/R injury.

The prefrontal cortex (PFC) constitutes a large part of the human central nervous system and is essential for the normal social affection and executive function of humans and other primates. Despite ongoing research in this region, the development of interactions between PFC genes over the lifespan is still unknown. To investigate the conversion of PFC gene interaction networks and further identify hub genes, we obtained time-series gene expression data of human PFC tissues from the Gene Expression Omnibus (GEO) database. A statistical model, loggle, was used to construct time-varying networks and several common network attributes were used to explore the development of PFC gene networks with age. Network similarity analysis showed that the development of human PFC is divided into three stages, namely, fast development period, deceleration to stationary period, and recession period. We identified some genes related to PFC development at these different stages, including genes involved in neuronal differentiation or synapse formation, genes involved in nerve impulse transmission, and genes involved in the development of myelin around neurons. Some of these genes are consistent with findings in previous reports. At the same time, we explored the development of several known KEGG pathways in PFC and corresponding hub genes. This study clarified the development trajectory of the interaction between PFC genes, and proposed a set of candidate genes related to PFC development, which helps further study of human brain development at the genomic level supplemental to regular anatomical analyses. The analytical process used in this study, involving the loggle model, similarity analysis, and central analysis, provides a comprehensive strategy to gain novel insights into the evolution and development of brain networks in other organisms.

Flavonoids are secondary metabolites that play important roles in fruit and vegetable development. Here, we examined the function of hyperoside, a unique flavonoid in okra (Abelmoschus esculentus), known to promote both flowering and seed set. We showed that the exogenous application of hyperoside significantly improved pollen germination rate and pollen tube growth by almost 50%, resulting in a 42.7% increase in the seed set rate. Of several genes induced by the hyperoside treatment, AeUF3GaT1, which encodes an enzyme that catalyzes the last step of hyperoside biosynthesis, was the most strongly induced. The transcription factor AeMYB30 enhanced AeUFG3aT1 transcription by directly binding to the AeUFG3aT1 promoter. We studied the effect of the hyperoside application on the expression of 10 representative genes at four stages of reproductive development, from pollination to seed maturity. We firstly developed an efficient transformation system that uses seeds as explants to study the roles of AeMYB30 and AeUFG3aT1. Overexpression of AeMYB30 or AeUF3GaT1 promoted seed development. Moreover, exogenous application of hyperoside partially restored the aberrant phenotype of AeUF3GaT1 RNA-interference plants. Thus, hyperoside promotes seed set in okra via a pathway involving AeUF3GaT and AeMYB30, and the exogenous application of this flavonoid is a simple method that can be used to improve seed quality and yield in okra.

Genome-wide association studies focusing on a single phenotype have been broadly conducted to identify genetic variants associated with a complex disease. The commonly applied single variant analysis is limited by failing to consider the complex interactions between variants, which motivated the development of association analyses focusing on genes or gene sets. Moreover, when multiple correlated phenotypes are available, methods based on a multi-trait analysis can improve the association power. However, most currently available multi-trait analyses are single variant-based analyses; thus have limited power when disease variants function as a group in a gene or a gene set. In this work, we propose a genome-wide gene-based multi-trait analysis method by considering genes as testing units. For a given phenotype, we adopt a rapid and powerful kernel-based testing method which can evaluate the joint effect of multiple variants within a gene. The joint effect, either linear or nonlinear, is captured through kernel functions. Given a series of candidate kernel functions, we propose an omnibus test strategy to integrate the test results based on different candidate kernels. A p-value combination method is then applied to integrate dependent p-values to assess the association between a gene and multiple correlated phenotypes. Simulation studies show a reasonable type I error control and an excellent power of the proposed method compared to its counterparts. We further show the utility of the method by applying it to two data sets: the Human Liver Cohort and the Alzheimer Disease Neuroimaging Initiative data set, and novel genes are identified. Our method has broad applications in other fields in which the interest is to evaluate the joint effect (linear or nonlinear) of a set of variants.

Atherosclerosis-induced cardiovascular diseases (CVDs) are accompanied by substantial morbidity and mortality. The loss and injury of endothelial cells is the primary cause of atherosclerosis. Rosuvastatin is an alternative agent used to reduce the risk of cardiovascular disease. Subsequently, the present study aimed to investigate the protective effects of rosuvastatin on oxidized-low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cell (HUVEC) injury. The viability of ox-LDL-cultured HUVECs with or without rosuvastatin (0.01, 0.1 and 1 µmol/l) pretreatment, and pretreatment at different time points (3, 6, 12 and 24 h) was determined using an MTT assay. Morphological changes and the extent of apoptosis were detected; the anti-oxidase activity, including superoxide dismutase (SOD) and catalase (CAT), was examined, and the contents of malondiahdehyde (MDA) and nitric oxide (NO) were measured. The phosphorylation levels of endothelial nitric oxide synthase (eNOS), protein kinase B (Akt) and phosphoinositide 3 kinase (PI3K) were detected using western blot analysis. The results demonstrated that pretreatment with 0.01–1 µmol/l rosuvastatin decreased cell apoptosis caused by ox-LDL. Notably, pretreatment with 1 µmol/l rosuvastatin for >12 h increased cell viability. Additionally, DAPI staining revealed that rosuvastatin inhibited HUVEC apoptosis. Rosuvastatin treatment also resulted in increased SOD and CAT activities and decreased MDA content in ox-LDL-stimulated HUVECs. Furthermore, pretreatment with 0.01–1 µmol/l rosuvastatin significantly increased` the NO content compared with HUVECs treated with ox-LDL alone. Western blot analyses demonstrated that rosuvastatin upregulated the phosphorylation of eNOS, Akt and PI3K. These findings indicated that rosuvastatin could protect HUVECs against ox-LDL-induced injury through its anti-oxidant effect and its ability to upregulate the expression of vascular endotheliocyte-protecting factors.

Actin depolymerising factor (ADF) is an actin binding protein that is ubiquitous in animal and plant cells. It plays an important role in plant growth and development, as well as resistance to biotic and abiotic stress. The research of plant ADF family has been restricted to Arabidopsis thaliana (L.) Heynh. and some herb crops, but no woody cash crops have been reported to date. All members of the Cajanus cajan (L.) Millsp. ADF (CcADF) family were identified from the pigeon pea genome, and distributed among the four subfamilies by phylogenetic analysis. CcADFs were relatively conservative in gene structure evolution, protein structure and functional expression, and different CcADFs showed specific expression patterns under different treatments. The expression characteristics of several key CcADFs were revealed by analysing the stress response pattern of CcADFs and the time series RNA-seq of aluminium stress. Among them, CcADF9 in the first subgroup specifically responded to aluminium stress in the roots; CcADF3 in the second subgroup intensively responded to fungal infection in the leaves; and CcADF2 in the fourth subgroup positively responded to various stress treatments in different tissues. This study extended the relationship between plant ADF family and aluminium tolerance, as well as adding to the understanding of CcADF family in woody crops.

Pigeonpea is an important economic crop in the world and is mainly distributed in tropical and subtropical regions. In order to further expand the scope of planting, one of the problems that must be solved is the impact of soil acidity on plants in these areas. Based on our previous work, we constructed a time series RNA sequencing (RNA-seq) analysis under aluminum (Al) stress in pigeonpea. Through a comparison analysis, 11,425 genes were found to be differentially expressed among all the time points. After clustering these genes by their expression patterns, 12 clusters were generated. Many important functional pathways were identified by gene ontology (GO) analysis, such as biological regulation, localization, response to stimulus, metabolic process, detoxification, and so on. Further analysis showed that metabolic pathways played an important role in the response of Al stress. Thirteen out of the 23 selected genes related to flavonoids and phenols were downregulated in response to Al stress. In addition, we verified these key genes of flavonoid- and phenol-related metabolism pathways by qRT-PCR. Collectively, our findings not only revealed the regulation mechanism of pigeonpea under Al stress but also provided methodological support for further exploration of plant stress regulation mechanisms.

Recently, several studies reported the association between miR-146a rs2910164 polymorphism and coronary artery disease (CAD) risk. However, the results were inconclusive. We therefore did a meta-analysis to investigate this association. Electronic databases, including PubMed, EMBASE, and China National Knowledge Infrastructure (CNKI) databases, were searched. The strength of association was assessed by calculating odds ratios (OR) and 95% confidence interval (CI). Five eligible studies included in this meta-analysis. The total sample size of this meta-analysis was 1565 cases and 1541 controls. We found that miR-146a rs2910164 polymorphism was significantly associated with an increased CAD risk (OR = 1.19; 95% CI 1.07 – 1.32; P = 0.002). In the subgroup analysis by race, miR-146a rs2910164 polymorphism was significantly associated with an increased CAD risk in Asians (OR = 1.18; 95% CI 1.04 – 1.33; P = 0.008). However, we did not find significant result in Caucasians (OR = 1.22; 95% CI 0.86 – 1.74; P = 0.25). In the subgroup analysis by age, we found that miR-146a rs2910164 polymorphism increased CAD risk in old population (OR = 1.22; 95% CI 1.09 – 1.38; P = 0.0008). In conclusion, this meta-analysis found that miR-146a rs2910164 polymorphism was significantly associated with CAD risk.

Background: Mutations in the solute carrier family 22 member 3 (SLC22A3), lipoprotein (a)-like 2 (LPAL2), and the lipoprotein (a) (LPA) gene cluster, which encodes apolipoprotein (a) [apo (a)] of the lipoprotein (a) [Lp (a)] lipoprotein particle, have been suggested to contribute to the risk of coronary artery disease (CAD), but the precise variants of this gene cluster have not yet been identified in Chinese populations. Objectives: We sought to investigate the association between SLC22A3-LPAL2-LPA gene cluster polymorphisms and the risk of CAD in the Han Chinese population. Patients and Methods: We recruited 551 CAD patients and 544 healthy controls for this case-control study. Four SNPs (rs9346816, rs2221750, rs3127596, and rs9364559) were genotyped in real time using the MassARRAY system (Sequenom; USA) in the SLC22A3-LPAL2-LPA gene cluster. All subjects were Chinese and of Han descent, and were recruited from the First Hospital of Jilin University based on convenience sampling from June 2009 to September 2012. Results: The frequency of the minor allele G (34.8%) in rs9364559 was significantly higher in the CAD patients than in the healthy controls (29.4%) (P = 0.006). There was genotypic association between rs9364559 and CAD (P = 0.022), and these results still remained significant after adjustment for the conventional CAD risk factors through forward logistic regression analysis (P = 0.020, P = 0.019). Haplotype analyses from different blocks indicated that 11 haplotypes were associated with the risk of CAD. Seven haplotypes were associated with a reduced risk of CAD, whereas four haplotypes were associated with an increased risk of CAD. Conclusions: Rs9364559 in the LPA gene may contribute to the risk of CAD in the Han Chinese population; haplotypes which contain rs9346816-G were all associated with an increased risk of CAD in this study.

Lp(a) has been well known as an independent risk factor for coronary artery disease (CAD). TheLPAgene, as it encodes apo(a) of the Lp(a) lipoprotein particle, was associated with increased risk of CAD. The purpose of this study was to analyze the relationship between the polymorphisms ofLPAgene and CAD in Chinese Han population. Five SNPs (rs1367211, rs3127596, rs6415085, rs9347438, and rs9364559) in theLPAgene were genotyped using Sequenom MassARRAY time-of-flight mass spectrometer (TOF) in 560 CAD patients as case group and 531 non-CAD subjects as control group. The numbers of these two groups were from Chinese Han ancestry. The results showed that allele (P=0.046) and genotype (P=0.026) of rs9364559 in theLPAgene was associated with CAD. The frequency of rs9364559 minor allele (G) in case group was obviously higher than that in control group. Results of haplotype analysis showed that 4 haplotypes which contained rs9364559-G were associated with increased risk of CAD in this population. This study explored rs9364559 in theLPAgene may be associated with the pathogenesis of CAD; and the risk of CAD might be higher in the population carrying 4 haplotypes of different blocks in theLPAgene.

The purpose of this study is to analyze the relationship between the polymorphisms of fatty acid desaturase 1 (FADS1), fatty acid desaturase 2 (FADS2), and elongation of very long-chain fatty acids-like 2 (ELOVL2) and acute coronary syndrome (ACS) in Chinese Han population. Therefore, we selected three single nucleotide polymorphisms (SNPs) from these candidate genes and genotyped them using PCR-based restriction fragment length polymorphism analysis in 249 ACS patients and 240 non-ACS subjects, as were Han Chinese ancestry. The results showed that rs174556 in theFADS1 gene is found to be in allelic association (P=0.003) and genotypic association (P=0.036) with ACS. The frequencies of rs174556 minor allele (T) in case group were obviously higher than in control group. The trans-phase gene-gene interaction analysis showed that the combined genotype of rs174556 (T/T) and rs3756963 (T/T) was associated with ACS (P=0.031). And the results suggest that, for rs174556 C>T, the CT/TT genotypes were more likely to lead in ACS in subjects with hypertension after correction of all risk factors (OR=4.236, 95% CI, 2.216–7.126). These findings suggest that the polymorphisms of rs174556 in theFADS1 gene are very likely to be associated with ACS in Chinese Han population, especially in subjects with hypertension.