Background The triglyceride-glucose (TyG) index is a new alternative measure for insulin resistance. This meta-analysis was conducted to assess the associations of the TyG index with the risks of cardiovascular diseases and mortality in the general population. Methods The PubMed, Cochrane Library and Embase databases were searched for randomized controlled trials or observational cohort studies reporting associations of the TyG index with cardiovascular diseases and mortality from inception to April 16, 2022. Effect sizes were pooled using random-effects models. Robust error meta-regression methods were applied to fit nonlinear dose–response associations. Evidence quality levels and recommendations were assessed using the Grading of Recommendations Assessment, Development and Evaluation system (GRADE). Results Twelve cohort studies (6 prospective and 6 retrospective cohorts) involving 6,354,990 participants were included in this meta-analysis. Compared with the lowest TyG index category, the highest TyG index was related to a higher incidence of coronary artery disease (CAD) (3 studies; hazard ratio [HR] = 2.01; 95% confidence interval [CI] 1.68–2.40; I2 = 0%), myocardial infarction (MI) (2 studies; HR = 1.36; 95% CI 1.18–1.56; I2 = 35%), and composite cardiovascular disease (CVD) (5 studies; HR = 1.46; 95% CI 1.23–1.74; I2 = 82%). However, there was no association between the TyG index and mortality (cardiovascular mortality [3 studies; HR = 1.10; 95% CI 0.82–1.47; I2 = 76%] or all-cause mortality [4 studies; HR = 1.08; 95% CI 0.92–1.27; I2 = 87%]). In the dose–response analysis, there was a linear association of the TyG index with the risk of CAD (Pnonlinear = 0.3807) or CVD (Pnonlinear = 0.0612). GRADE assessment indicated very low certainty for CVD, MI, cardiovascular mortality and all-cause mortality, and moderate certainty for CAD. Conclusions Based on our current evidence, a higher TyG index may be associated with an increased incidence of CAD (moderate certainty), MI (very low certainty) and CVD (very low certainty) in the general population. There is a potential linear association of the TyG index with CAD and the composite CVD incidence. Further prospective studies (especially in non-Asians) are needed to confirm our findings.
Cardiac microvascular endothelial cells (CMECs) dysfunction induced by hypoxia is an important pathophysiological event in myocardium ischemic injury, whereas, the underlying mechanism is not fully clarified. FoxO transcription factors regulate target genes involved in apoptosis and cellular reactive oxygen species (ROS) production. Therefore, the present study was designed to elucidate the potential role of FoxOs on the hypoxia-induced ROS formation and apoptosis in CMECs. Exposure to low oxygen tension stimulated ROS accumulation and increased apoptosis in CMECs within 6–24 h. Hypoxia also significantly increased the expressions of HIF-1α and FoxO3a. However, hypoxia decreased the phosphorylation of Akt and FoxO3a, correlated with increased nuclear accumulation. Conversely, the expression of FoxO1 was not significantly altered by hypoxia. After inhibition of HIF-1α by siRNA, we observed that hypoxia-induced ROS accumulation and apoptosis of CMECs were decreased. Meanwhile, knockdown of HIF-1α also inhibited hypoxia induced FoxO3a expression in CMECs, but did not affect FoxO1 expression. Furthermore, hypoxia-induced ROS formation and apoptosis in CMECs were correlated with the disturbance of Bcl-2 family proteins, which were abolished by FoxO3a silencing with siRNA. In conclusion, our data provide evidence that FoxO3a leads to ROS accumulation in CMECs, and in parallel, induces the disturbance of Bcl-2 family proteins which results in apoptosis.
BackgroundThe objective of this study was to investigate the molecular mechanism of atrial fibrillation (AF), as well as the negative regulatory relationship between miR-29a-3p and CACNA1C.Material/MethodsWe searched the online miRNA database (www.mirdb.org) and identified the miR-29a-3p binding sequence within the 3′-UTR of the target gene, and then conducted luciferase assay to verify it. The cells were transfected with miR-29a-3p and ICa,L was determined in those cells.ResultsWe validated CACNA1C to be the direct target gene of miR-29a-3p. We also established the negative regulatory relationship between miR-29a-3p and CACNA1C via studying the relative luciferase activity. We also conducted real-time PCR and Western blot analysis to study the mRNA and protein expression level of CACNA1C among different groups of cells treated with scramble control, 30nM miR-29a-3p mimics, and 60nM miR-29a-3p mimics, indicating a negative regulatory relationship between miR-29a-3p and CACNA1C. We next analyzed whether miR-29a-3p transfection in cardiomyocytes produced the effects on the ICa,L induced by electrical remodeling, and found a tonic inhibition of IBa by endogenous miR-29a-3p in atrial myocytes.ConclusionsWe validated the negative regulation between miR-29a-3p and CACNA1C, and found that miR-29a-3p might a potential therapeutic target in the treatment of AF.
BackgroundDisrupted circadian rhythm of blood pressure is commonly observed in patients in the intensive care unit (ICU). This study assessed the association of nocturnal mean arterial pressure rising (NMAPR) with short‐ and long‐term mortality in critically ill adult patients.Methods and ResultsAdult patients with a complete record of mean arterial pressure monitoring during the first 24 hours of ICU stay in the Multiparameter Intelligent Monitoring in Intensive Care II (MIMIC‐II) database were included in this retrospective cohort study. All patients were divided into the non‐NMAPR group (≤1) or the NMAPR group (>1), according to the value of mean nighttime divided by daytime mean arterial pressure. The associations of NMAPR with ICU, hospital, 28‐day, and 1‐year mortality were assessed using multivariable logistic regression or a Cox proportional hazards model. Interaction and subgroup analyses were performed for those patients who had a first Sequential Organ Failure Assessment (SOFA) score of ≥8 or <8. The overall cohort comprised 5185 patients. The patients with NMAPR (n=1865) had higher ICU, hospital, 28‐day, and 1‐year mortality than the non‐NMAPR group (n=3320). After adjusting for covariates, the analysis showed that NMAPR was significantly associated with mortality in the ICU (odds ratio: 1.34; 95% CI, 1.10–1.65), in the hospital (odds ratio: 1.35; 95% CI, 1.12–1.63), at 28 days (hazard ratio: 1.27; 95% CI, 1.10–1.48), and at 1 year (hazard ratio: 1.24; 95% CI, 1.10–1.40). All results of the interaction analysis had no statistical significance, and similar results persisted in the patients with different SOFA scores.Conclusions NMAPR may aid in the early identification of critically ill patients at high risk of ICU, hospital, 28‐day, or 1‐year mortality.
ABSTRACT.A case-control study was conducted to investigate the association between genetic variants of IL-17A rs2275913 and IL-17F rs763780 and the development of coronary artery disease (CAD) in a Chinese population. A total of 306 individuals with CAD and 306 unaffected individuals were enrolled from the Zhengzhou People's Hospital between May 2012 and May 2014. The IL-17A rs2275913 and IL-17F rs763780 genes were genotyped by polymerase chain reaction combined with a restriction fragment length polymorphism (PCR-RFLP). Logistic regression analysis revealed that individuals with the AA genotype of rs2275913 were associated with increased risk of CAD, compared to those with the GG genotype in a codominant model [adjusted odds ratio (OR) = 1.96; 95% confidence interval (CI) = 1.10-3.53]. On the other hand, the AA genotype of rs2275913 was correlated with moderately increased risk of CAD compared to the GG + GA genotype (adjusted OR = 1.76; 95%CI = 1.02-3.07) in a recessive model. However, no significant differences were observed between polymorphisms at the IL-17F rs763780 locus and CAD risk, in codominant, dominant, and recessive models. In conclusion, the results of our study suggested that the IL-17A rs2275913 polymorphism may affect the development of CAD; however, no significant association was observed between the IL-17F rs763780 polymorphism and risk of CAD.
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