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The dried bulbs of Allii Macrostemonis Bulbus (AMB) are called "薤白" in China and are mainly distributed in Asia. The plant species included in the 2020 Edition of the Chinese Pharmacopoeia (ChP) are Allium macrostemon Bunge (called xiaogensuan in Chinese, A. macrostemon) and Allium chinense G. Don (called xie in Chinese, A. chinense), respectively. In the traditional Chinese medicine (TCM) theoretical system, AMB is warm in nature, acrid-bitter taste, and attributive to the heart, lung, stomach, large intestine meridian. AMB has the function of activating Yang and removing stasis, regulating Qi and eliminating stagnation. Modern pharmacological studies have shown that AMB has anti-platelet aggregation, hypolipidemic, anti-atherosclerotic, cardiomyocyte, vascular endothelial cell protection, anti-cancer, anti-bacterial, anti-asthmatic, and anti-oxidant effects. In some Asian countries, AMB is often used to treat coronary heart disease (CHD), angina pectoris (AP), asthma, and diarrhea. This review collates the botanical background, ethnopharmacology, phytochemistry, pharmacological activities, quality control, and toxicological studies of AMB, and provides an outlook on the current research deficiencies and future research priorities of AMB, intending to provide ideas for future research directions and commercial development. [ABSTRACT FROM AUTHOR]

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Epidemiological studies have shown that the incidence, prevalence and mortality of atherosclerotic cardiovascular disease (ASCVD) are increasing globally. Atherosclerosis is characterized as a chronic inflammatory disease which involves inflammation and immune dysfunction. P. lactiflora Pall. is a plant origin traditional medicine that has been widely used for the treatment of various diseases for more than a millennium in China, Japan and Korean. Paeoniflorin is a bioactive monomer extracted from P. lactiflora Pall. with antiatherosclerosis effects. In this article, we comprehensively reviewed the potential therapeutic effects and molecular mechanism whereby paeoniflorin protects against atherosclerosis from the unique angle of inflammation and immune-related pathway dysfunction in vascular endothelial cells, smooth muscle cells, monocytes, macrophages, platelets and mast cells. Paeoniflorin, with multiple protective effects in atherosclerosis, has the potential to be used as a promising therapeutic agent for the treatment of atherosclerosis and its complications. We conclude with a detailed discussion of the challenges and future perspective of paeoniflorin in translational cardiovascular medicine. [ABSTRACT FROM AUTHOR]

The incidence of pregnancy-induced hypertension in China is 9.4%, which is at a relatively high level. Its serious impact on maternal and infant health is the main reason for maternal and perinatal morbidity and mortality. There are many factors affecting pregnancy-induced hypertension. The incidence of pregnancy-induced hypertension is different due to different levels of cultural knowledge, health awareness, economic income, nutrition, and medical support. Since its etiology has not been elucidated thus far, there is no known treatment of the disease, and the main principles are spasmolysis, hypotension, expansion, and timely termination of pregnancy. Observe the effect of nimodipine combined with magnesium sulfate on serum heat shock protein 70 (HSP70) and pentamer 3 (PTX3) levels in patients with pregnancy-induced hypertension. Ninety-six patients with pregnancy-induced hypertension syndrome admitted to our hospital from May 2016 to February 2019 are selected and randomly divided into two groups according to the 1 : 1 principle, with 48 cases in each group. The single drug group is treated with magnesium sulfate, and the combined group is treated with nimodipine combined with magnesium sulfate. Changes in blood pressure, HSP70, PTX3, placental growth factor (PLGF), and vascular endothelial cell injury markers are recorded in the two groups, and adverse reactions and pregnancy outcomes are observed. After treatment, the blood pressure and levels of HSP70, PTX3, endothelin-1 (ET-1), and nitric oxide (NO) in the two groups decreased, and the level of PLGF increased. The diastolic blood pressure, systolic blood pressure, and levels of HSP70, PTX3, ET-1, and NO in the combined group are lower than those in the single drug group, and the level of PLGF is higher than that in the single drug group (P < 0.05). During the treatment period, the adverse reaction rate of the combined group is 6.25% compared with 8.33% of the single agent group, and the difference is not statistically significant (P > 0.05). Follow-up visits found that the cesarean section rate and abnormal fetal heart rate in the combined group are 16.67% and 4.17%, respectively, which are lower than 35.42% and 16.67% in the single drug group, and the difference is statistically significant (P < 0.05). Compared with 14.58%, 12.50%, and 2.08% in the single drug group, the neonatal asphyxia rate, premature birth rate, and stillbirth rate in the combined group are 6.25%, 4.17%, and 0.00%, respectively, and the difference is not statistically significant (P > 0.05). Nimodipine combined with magnesium sulfate can effectively control blood pressure in patients with pregnancy-induced hypertension, reduce vascular endothelial damage, regulate the expression of HSP70, PTX3, and PLGF, and improve pregnancy outcomes without increasing adverse reactions. [ABSTRACT FROM AUTHOR]

Calcium, as a second messenger, plays an important role in the pathogenesis of cardiovascular diseases (CVDs). The malfunction of calcium signaling in endothelial cells and vascular smooth muscle cells promotes hypertension. In cardiomyocytes, calcium overload induces apoptosis, leading to myocardial infarction and arrhythmias. Moreover, the calcium–calcineurin–nuclear factor of activated T cells (NFAT) pathway is essential for expressing the cardiac pro-hypertrophic gene. Heart failure is also characterized by reduced calcium transient amplitude and enhanced sarcoplasmic reticulum (SR) calcium leakage. Traditional Chinese medicine (TCM) has been used to treat CVDs for thousands of years in China. Because of its multicomponent and multitarget characteristics, TCM's unique advantages in CVD treatment are closely related to the modulation of multiple calcium handling proteins and calcium signaling pathways in different types of cells involved in distinct CVDs. Thus, we systematically review the diverse mechanisms of TCM in regulating calcium pathways to treat various types of CVDs, ranging from hypertrophic cardiomyopathy to diabetic heart disease. [ABSTRACT FROM AUTHOR]

Liver cancer is one of the most frequent causes of cancer-related deaths worldwide. The current study sought to screen, for the first time, a Ficus carica variety from the Shandong province of China against hepatocellular (HepG2) cells. Crude extracts of F. carica with various polarities were prepared and screened against HepG2 cells. The acetone extract of the leaf (FLA) exhibited significant antiproliferative effects against HepG2 cells (IC 50 = 0.179 mg/mL) while producing the least toxicity on normal human umbilical vein endothelial cells (HUVECs). Biochemical evidence of apoptosis was confirmed by staining with DAPI and AO/EB. FLA also exhibited moderate anti-colonization potential against the population of HepG2 cells. It selectively arrested the cell cycle of HepG2 cells at the S phase and exerted anticancer activity by significantly increasing the reactive oxygen species (1.59 fold) inside the cells, which subsequently resulted in loss of the mitochondrial membrane potential as revealed by JC-1 probe assay. FLA downregulated the expression of tumor-promoter Transcription Factor (TP53), anti-apoptotic proteins (Bcl-2), and cell cycle regulatory kinases (CDK1, 5, 9) with respect to untreated cells for 24 h, 48 h, and 72 h. High-performance liquid chromatography (HPLC) of FLA revealed the presence of gallic acid and quercetin as major antiproliferative compounds along with trace amounts of rutin, luteolin, apigenin, benzoic acid, and β-sitosterol. Notably, our study showed FLA operating via novel mechanisms involving reactive oxygen species (ROS) generation and CDKs involvement in HepG2 cells. Thus, it suggests that FLA may be a potential source of new drugs in the treatment of liver cancer. [Display omitted] • Acetone based extract from Ficus carica proved most cytotoxic against HepG2 cells. • Extract proved least toxic against human umbilical derived vascular endothelial cells. • Upsurge of reactive oxygen species and inactivated mitochondrial membrane potential-modes of apoptosis. • Alleviation in TP53, Bcl-2 and CDK1, CDK5 and CDK9 genes; induction of apoptosis. • The gallic acid and quercetin found as major compounds in active extract. [ABSTRACT FROM AUTHOR]

SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2), emerging in Wuhan city, China, causing COVID-19 disease, has been described as a pandemic by WHO (World Health Organization), leading to outbreaks of pneumonia. The COVID-19 pandemic continues to affect millions of people worldwide. SARSCOV- 2 enters the cell via ACE-2 (Angiotensin-converting enzyme 2) receptor. These receptors are predominantly found in lung, small intestine, and vascular endothelial cells. Since ACE 2 is found more frequently in these tissues, common clinical symptoms include fever, cough, sore throat, fatigue, dyspnea, and diarrhea. Currently, although symptomatic treatments are applied for COVID-19, there is no specific treatment yet. It takes a long time before targeted therapies can be found. For this reason, it is necessary to develop emergency treatment or methods that can quickly control the disease. Phytotherapeutic compositions offer a potentially valuable resource for this purpose. Many countries, especially China, aimed to reduce morbidity and mortality by using phytotherapy throughout COVID-19 patients. Phytotherapeutic products are known to be safe and tolerable with their background knowledge. In this regard, the use of phytotherapy as a complementary treatment in COVID-19 patients is very important. In this review, phytotherapeutic approaches related to symptoms that may occur in the clinical course of COVID-19 disease will be discussed. [ABSTRACT FROM AUTHOR]

Anlotinib hydrochloride is a multi-target tyrosine kinase inhibitor, which has been recently approved for the treatment of advanced non-small cell lung cancer in China. One of its mechanisms of action is the inhibition of angiogenesis and it is similar to other anti-angiogenesis drugs, as it has cardiovascular toxicity, which may damage vascular endothelial cells and result in hypertension and hyperlipidemia. All of the aforementioned factors are considered risk factors for coronary heart disease; however, the risk of developing acute myocardial infarction (AMI) has not been assessed by any previous clinical trials and subsequent research. The present case study, to the best of our knowledge, was the first to report on a patient who developed hypertension, hyperlipidemia and angina pectoris, and eventually experienced AMI, following treatment with anlotinib. This indicates that patients receiving anlotinib may require further observation and monitoring during use. [ABSTRACT FROM AUTHOR]

Hantaviruses can cause hemorrhagic fever with renal syndrome (HFRS) in Eurasia and have led to public health threat in China. The pathogenesis of HFRS is complex and involves capillary leakage due to the infection of vascular endothelial cells. Accumulating evidence has demonstrated that hantavirus can induce apoptosis in many cells, but the mechanism remains unclear. Our studies showed that Hantaan virus (HTNV) infection could induce TNF-related apoptosis-inducing ligand (TRAIL) expression in primary human umbilical vein endothelial cells (HUVECs) and sensitize host cells toward TRAIL-mediated apoptosis. Furthermore, TRAIL interference could inhibit apoptosis and enhance the production of HTNV as well as reduce IFN-β production, while exogenous TRAIL treatment showed reverse outcome: enhanced apoptosis and IFN-β production as well as a lower level of viral replication. We also observed that nucleocapsid protein (NP) and glycoprotein (GP) of HTNV could promote the transcriptions of TRAIL and its receptors. Thus, TRAIL was upregulated by HTNV infection and then exhibited significant antiviral activities in vitro , and it was further confirmed in the HTNV-infected suckling mice model that TRAIL treatment significantly reduced viral load, alleviated virus-induced tissue lesions, increased apoptotic cells, and decreased the mortality. In conclusion, these results demonstrate that TRAIL-dependent apoptosis and IFN-β production could suppress HTNV replication and TRAIL treatment might be a novel therapeutic target for HTNV infection. [ABSTRACT FROM AUTHOR]

Context: Ferulic acid (FA) is an active principle derived from the traditional Chinese medicine Angelica sinensis, which has been used for the treatment of cardiovascular and cerebrovascular diseases in China for many years. However, a thorough understanding of effects on vascular function by FA has not been investigated. Aims: The aim of the present study was to investigate the potential mechanism of FA by suppressing Transient receptor potential cation channel subfamily M member 8 (TRPM8) channels and regulating endothelial nitric oxide (NO) pathway to ameliorate cold explore injury in human umbilical vascular endothelial cells (HUVECs). Subjects and Methods: The effects of cold exposure and FA on cell viability were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and lactate dehydrogenase (LDH) assay. Quantitative polymerase chain reaction and Western blot were utilized to detect TRPM8, hypoxia-inducible factor-alpha (HIF-1α), endothelin-1 (ET-1), inducible NO synthase (iNOS), endothelial NO synthase (eNOS) messenger RNA, and protein expression in HUVECs. Enzyme-linked immunosorbent assay method was used to detect the concentration of ET-1 in culture supernatants of HUVECs. Results: Cold exposure at 18°C had no significant effect on cell morphology but increased secretion of LDH and ET-1 and the expression of TRPM8, HIF-1α, iNOS, and ET-1. Treatment with FA decreased all of these changes. The levels of NO and eNOS decreased in cold stress model, while FA treatment attenuated the cold-induced decrease of NO and eNOS. Conclusion: Cold stress can cause an increase in vasoconstrictors such as TRPM8 and ET-1 and reducing cell viability, but FA can prevent cold stress-related cardiovascular disease by regulating the expression of these substances in cells. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) is the leading cause of death globally and poses at significant challenge in terms of effective medical treatment. Leonurus japonicus Houtt , a traditional Chinese herb, is widely used in China for the treatment of obstetrical and gynecological disorders, including menstrual disorders, dysmenorrhea, amenorrhea, blood stasis, postpartum bleeding, and blood-related diseases such as CVD. Stachydrine, the main alkaloid component of Leonurus, has been shown to exhibit a wide range of biological activities including anti-inflammatory, antioxidant, anti-coagulant, anti-apoptotic, vasodilator, angiogenic promoter. Additionally, it has been demonstrated to have unique advantages in the prevention and treatment of CVD through regulation of various disease-related signaling pathways and molecular targets. In this comprehensive review, we examine the latest pharmacological effects and molecular mechanisms of Stachydrine in treating cardiovascular and cerebrovascular diseases. Our aim is to solid scientific basis for the development of new CVD drug formulations. [Display omitted] • 1 STA can protect vascular endothelial cells from damage. • 2 STA can help to prevent cardiovascular disease (CVD) by inhibiting cardiomyocyte hypertrophy, cardiomyocyte fibrosis, and anti-apoptosis. • 3 STA can also protect Central Nervous System (CNS) diseases, such as protect traumatic brain injury and Alzheimer's disease. • 4 STA has properties of good bioavailability, non-toxic and very low toxicity. [ABSTRACT FROM AUTHOR]

Objective: To observe the time-effect relation of extracts from ginseng, notoginseng and chuanxiong on angiotensin II (Ang II)-induced senescence of vascular endothelial cells and explore the feature of Chinese medicine against vascular diseases. Methods: Human umbilical vein endothelial cells (HUVECs) cultured in vitro were stimulated with 10 mol/L AngII to induce cell senescence, which were divided into 4 groups, the blank control group, the Ang II model group, the extracts group and the telmisartan group. The β-gal was used to identify senescence of cells, the cell counting kit-8 method was applied to assess the cell viability, the cell function was examined with the level of endothelial nitric oxide synthase (eNOS) and the flow cytometry was used for analyzing the cell cycle changes. Results: Compared with the control cells, the cells positive for β-gal staining was significantly increased in the Ang II model group, and showed cell cycle arrest at G/G phase with decreased S and G/M phase cell percentage, eNOS expression and cell viability ( P<0.05). The extracts and telmisartan treatment of Ang II-induced cells resulted in decreased β-gal positive cells with a reduction in G/G phase cells and an increasing in S, G/M phase cells and eNOS expression ( P<0.05). At 24 h, the extracts were more effective than telmisartan ( P<0.05); while telmisartan was more effective at 48 h ( P<0.05). Conclusion: Extracts from ginseng, notoginseng and chuanxiong can delay Ang II-induced aging of HUVECs and may play an important role in early senescence. [ABSTRACT FROM AUTHOR]

Epidemiological studies have shown that cardiovascular diseases caused by PM 2.5 pollution account for the second death rate in China. Polycyclic aromatic hydrocarbons (PAHs) are one important group of persistent organic pollutants absorbed on PM 2.5. Though individual PAH is related to vascular disease, the relationship between environmental PAHs exposure and vascular damages is still unclear. To explore the effect of PAHs on blood vessel, human umbilical vein endothelial cells (HUVECs) are treated with 16 priority–controlled PAHs at various concentrations to study their cytotoxicity and morphological alteration. Results showed that, after 48 h treatment, PAHs mixture generally attenuated the ability of wound healing, transwell migration and tube formation of HUVECs (p < 0.01) except for 1 × PAHs in transwell migration. Moreover, PAHs increased the levels of ROS and 8-hydroxy-2′-deoxyguanosine (p < 0.05), indicating that it exceeded the scavenging ability of superoxide dismutase activity. However, PAHs mixture did not increase apoptosis rate, which may be attribute to the difference of PAH concentration and composition between this study and previous reports. Downstream signaling cascades significantly and generally upregulated the relative expression of proteins in Nrf2/HO-1 and NF-ƙB/TNF- α pathway with the activation of oxidative stress, including HO-, TNF- α and Nrf2. In summary, this study suggests that environmental mixture of 16 priority-controlled PAHs can induce the damages of vascular endothelial cells involved in cellular oxidative stress and inflammation. [Display omitted] • Environmental dose PAHs mixture can induce the damages of HUVECs. • Oxidative stress and inflammation involve the damages of HUVECs exposed to PAHs. • PAHs may be the dominant compounds on PM 2.5 which increase the occurrence of CVD. [ABSTRACT FROM AUTHOR]

China's tilapia industry has the most complete industrial chain in the world, but, in recent years, tilapia streptococcosis have frequently occurred, which has become a bottleneck restricting the development of tilapia industry. Although plenty of studies have been conducted on Streptococcus agalactiae (Group B Streptococcus , GBS) in tilapia, the mechanism of GBS invasion is still unclear. In order to further understand the invasion route, we used the qPCR method to study bacteria load in liver, intestine, gill, spleen, head kidney, kidney, and brain tissues of GIFT tilapia infected by a GBS virulent strain WC1535 at different infection time and the histological method to systematically analyze bacterial distribution and localization in above infected tissue. Through the dynamic analysis of bacteria load, the bacterial copy number of WC1535 reached the peak in each tissue at 24 h post-infection (hpi). Therefore, tissues at 24 hpi were taken as the research object to investigate the distribution and localization of WC1535 by paraffin section and electron microscopy. The results of tissue section showed that WC1535 existed in three forms in blood: free scattering without attachment to any structure, phagocytized by phagocytes (mainly macrophages) and a few red blood cells, and attached to the inner wall of blood vessels. The results of qPCR and tissue section both showed that the density of bacteria in head kidney, spleen and gill was high, at the same time, these tissues had abundant blood and capillaries, so this suggested that the S. agalactiae existed mainly in the blood of tilapia. There were almost no pathogens in the parenchymal cells of each tissue, but the surface of epithelial cells such as vascular endothelial cells and fibroblasts adhered a lot, which indicated that S. agalactiae had epithelial cell affinity. The results of electron microscopy showed that S. agalactiae can survive and proliferate intracellularly after being phagocytosed by macrophages, suggesting that macrophages might play as pathogen carriers or "Trojan horses" to achieve the immune escape, break the blood-brain barrier (BBB), and lead the meningitis in tilapia. Since GBS of tilapia can be internalized by macrophages, antibiotics with strong tissue distribution, cell penetration and good meningeal penetration are recommended for the treatment in the early stage of streptococcosis. • S. agalactiae strain WC1535 was widely distributed in different tissues of tilapia. • WC1535 distribution in tilapia had the characteristic of epithelial cell affinity. • WC1535 cells could localize and proliferate in the macrophages of tilapia. • The endocytic WC1535 in macrophages were surrounded by the membrane structure. • Histological evidence for breaking the blood-brain barrier of S. agalactiae. [ABSTRACT FROM AUTHOR]

Endothelial cell dysfunction is considered to be one of the major causes of vascular complications in diabetes. Polyphenols are known as potent antioxidants that can contribute to the prevention of diabetes. Corn silk has been reported to contain polyphenols and has been used in folk medicine in China for the treatment of diabetes. The present study aims to investigate the potential protective role of the phenolic-rich fraction of corn silk (PRF) against injuries to vascular endothelial cells under high glucose conditions in vitro and in vivo. The protective effect of PRF from high glucose toxicity was investigated using human umbilical vein endothelial cells (HUVECs). The protective effect of PRF was subsequently evaluated by using in vivo methods in streptozotocin (STZ)-induced diabetic rats. Results showed that the PRF significantly reduced the cytotoxicity of glucose by restoring cell viability in a dose-dependent manner. PRF was also able to prevent the histological changes in the aorta of STZ-induced diabetic rats. Results suggested that PRF might have a beneficial effect on diabetic patients and may help to prevent the development and progression of diabetic complications such as diabetic nephropathy and atherosclerosis. [ABSTRACT FROM AUTHOR]

Background: BRD4 and PIN1 have been described to be involved in inflammation and vascular endothelial cell dysfunction, which in turn may increase pulse pressure.Hypothesis: Genetic mutations within the BRD4 and PIN1 genes could affect the risk of high pulse pressure.Methods: A total of four single nucleotide polymorphisms (SNPs) (BRD4: rs4808278; PIN1: rs2233678, rs2287838, and rs2233682) were genotyped in a cohort of 666 hypertensive patients and 232 normotensive controls with Chinese Han origin. Generalized multifactor dimensionality reduction (GMDR) was used to screen the best interaction combination among the four SNPs within the BRD4 and PIN1 genes and diabetes. Logistic regression analysis was performed to calculate the odds ratio (ORs) (95% confidence interval (CI)) for the association between the four SNPs.Results: Adjusted for age, weight, waist circumference, drinking, smoking, hypertension, and diabetes, high pulse pressure risk was significantly higher for carriers with the rs4808278-TT genotype in BRD4 than those with wild genotypes (OR: 0.400, 95% CI: 0.217-0.737, P* < 0.05). However, we did not find any significant association of rs2233678, rs2287838, and rs2233682 in PIN1 with high pulse pressure susceptibility after covariate adjustment. GMDR analysis indicated a significant three-locus model (P = 0.0107) involving rs4808278, rs2233678, and diabetes, the cross-validation consistency of the three-locus models was 9/10, and the testing accuracy was 57.47%.Conclusions: Genetic mutations within BRD4 (rs4808278) could affect the susceptibility to high pulse pressure in a southeastern Chinese population. [ABSTRACT FROM AUTHOR]

Aims: Coronary heart disease (CHD), a chronic inflammatory condition of vascular endothelial cells (VECs), poses a serious threat to human health. Previous studies have found that microRNAs (miRNAs) are closely related to the occurrence and development of cardiac diseases. Therefore, this study focused on the regulation by miR-323-3p on the progression of CHD., Methods: Initially, we employed microarray-based gene expression profiling of CHD to identify differentially expressed miRNAs. Next, the expression of miR-323-3p and SIRT1 was detected by RT-qPCR in a rat model of CHD generated by feeding with a high-fat diet. The interaction between miR-323-3p and SIRT1 was identified using bioinformatics analysis and dual luciferase reporter gene assay. The expressions of miR-323-3p and SIRT1 were altered in CHD rats and vascular endothelial cells (VECs) to examine the specific effects on CHD., Results: miR-323-3p was observed to be highly-expressed in blood samples from patients with CHD or with mild atherosclerosis and in the rat model of CHD. SIRT1 was a target gene of miR-323-3p, which could downregulate SIRT1 expression. miR-323-3p overexpression or SIRT1 inhibition resulted in increased apoptosis of VECs, elevated ac-p65 protein expression and ratio of ac-p65/p65, and upregulated expression of NF-κB signaling pathway-related proteins. Besides, miR-323-3p inhibition or SIRT1 upregulation in the CHD rat model was found to significantly alleviate symptoms and decrease levels of proteins related to the ac-p65 and NF-κB signaling pathways., Conclusion: Overall, the experimental data provide evidence that miR-323-3p suppression may restrain VEC apoptosis and prevent the resultant CHD progression via SIRT1-inactivatedNF-κB signaling pathway., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: Endothelin (ET)‐1 is a potent vasoconstrictor peptide produced by endothelial cells and associated with vascular dysfunction and cardiovascular disease. Lys198Asn is a single‐nucleotide polymorphism (SNP) of gene encoding ET‐1 (EDN1). It is hypothesized that it might have a role in altering ET‐1 and ultimately leading to vascular dysfunction and ischemic stroke. We therefore conducted a meta‐analysis to investigate the association between Lys198Asn polymorphism of EDN1 gene and susceptibility of ischemic stroke. Methods: This meta‐analysis was conducted according to the guidance of the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) statement. We searched PubMed, Google Scholar, Embase, Web of Science, J‐STAGE, and China National Knowledge Infrastructure (CNKI) for relevant studies. The association between Lys198Asn polymorphism and ischemic stroke susceptibility was evaluated by calculating the pooled ORs and 95% CIs. Results: Our analysis included 1,291 cases and 2,513 controls. Meta‐analysis established a significant association between Lys198Asn SNP of EDN1 gene and ischemic stroke when assuming either recessive model (OR: 1.30; 95% CI: 1.02–1.65; p = .03; I2 = 41%) or dominant model (OR: 1.48; 95% CI: 1.24–1.76; p < .001; I2 = 61%). There was no evidence of publication bias in either of the recessive model (Egger test: p = .23; Begg test: p = .85) or dominant model (Egger test: p = .79; Begg test: p = .85). A subgroup analysis based on subtypes of ischemic stroke showed that Lys198Asn SNP was only associated with large vessel infarction but not with lacunar infarction caused by small vessel disease. A subgroup analysis based on ethnicity revealed that the Lys198Asn polymorphism of the EDN1 gene was associated with ischemic stroke only in Caucasians. Conclusions: The present meta‐analysis suggests that Lys198Asn polymorphism of EDN1 gene is associated with an increased risk for ischemic stroke. [ABSTRACT FROM AUTHOR]

Background: Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) plays an important role in vascular remodeling. Down-regulation of MALAT1 can inhibit the proliferation of vascular endothelial cells and vascular smooth muscle cells, reduce cardiomyocyte apoptosis and improve left ventricular function, which is closely linked to numerous pathological processes such as coronary atherosclerotic heart disease (CAD). The aim of this study was to investigate whether polymorphisms in MALAT1 were associated with the susceptibility to CAD. Methods: A total of 508 CAD patients and 562 age-, gender-, and ethnicity-matched controls were enrolled in this study. Four polymorphisms in MALAT1 (i.e., rs11227209, rs619586, rs664589, and rs3200401) were genotyped using a TaqMan allelic discrimination assay. Results: The rs619586 AG/GG genotypes and G allele were associated with a reduced risk of CAD (AG/GG vs. AA: adjusted OR = 0.66, 95% CI: 0.48–0.91; G vs. A: adjusted OR = 0.68, 95% CI: 0.51–0.90). Stratification analyses showed that CAD patients with rs11227209 CG/GG, rs619586 AG/GG, and rs3200401 CT/TT genotypes exhibited lower levels of TCH (P = 0.02, 0.04, and 0.02, respectively). Moreover, CGCC haplotype was associated with a decreased risk of CAD (OR = 0.28, 95% CI: 0.16–0.48). Multivariate logistic regression analysis identified some independent risk factors for CAD, including rs619586 and rs664589. Subsequent combined analysis showed that the combined genotypes of rs619586AG/GG and rs664589CC were associated with a reduced risk of CAD (OR = 0.29; 95%CI, 0.16–0.53). Conclusions: These findings indicate that rs619586AG/GG genotypes in MALAT1 may protect against the occurrence of CAD. [ABSTRACT FROM AUTHOR]