This study aimed to explore the association between dietary fiber intake and hypertension risk using 2017 American College of Cardiology/American Heart Association Blood Pressure Guidelines. Data from the National Health and Nutrition Examination Survey 2007–2014 were used in this study. Dietary fiber data were obtained through two 24-h dietary recall interviews. Hypertension was defined as systolic blood pressure (SBP) ≥ 130 mmHg or diastolic blood pressure (DBP) ≥ 80 mmHg or treatment with hypertensive medications. Logistic regression models and restricted cubic spline models were applied to evaluate the associations between dietary intakes of total, cereal, vegetable, and fruit fiber and hypertension. A total of 18,433 participants aged 18 years or older were included in the analyses. After adjustment for age, gender, body mass index (BMI), race, educational level, smoking status, family income, and total daily energy intake, compared with the lowest tertile, the odds ratios (95% confidence intervals) of hypertension for the highest tertile intakes of total, cereal, vegetable, and fruit fiber were 0.62 (0.52–0.75), 0.80 (0.67–0.96), 0.82 (0.69–0.98), and 0.86 (0.71–1.04), respectively. Dose-response analyses revealed that the risk of hypertension was associated with total fiber intake in a nonlinear trend, while the relationships were linear for cereal and vegetable fiber intakes. Our results suggested that the intakes of total, cereal, and vegetable fiber, but not fruit fiber, were associated with a decreased risk of hypertension in U.S. adults.

We conducted this cross-sectional study in the American general population to explore the association of dietary n3 and n6 fatty acids intake and the risk of hypertension. We used data from the National Health and Nutrition Examination Survey (NHANES) 2007–2014 in this study. We obtained dietary n3 and n6 fatty acids data through two 24 h dietary recall interviews and n3, n6 fatty acids intake were adjusted by weight. We defined hypertension as now taking prescribed medicine for hypertension or blood pressure above 130/80 mmHg. We applied binary logistic regression, multinomial logistic regression, and restricted cubic spline to evaluate the associations of dietary n3 and n6 fatty acids intake with hypertension. A total of 18,434 participants were included in this study. In the multivariate-adjusted model 2, the odds ratios (ORs) with 95% confidence interval (CI) of hypertension were 0.58 (0.49–0.68), 0.53 (0.45–0.63), and 0.92 (0.80–1.06) for the highest versus the lowest tertile of dietary n3, n6 fatty acids intake and n6:n3 ratio, respectively. Further excluded participants with hypertension history, the ORs with 95% CI of newly diagnosed hypertension were 0.60 (0.50–0.73), 0.52 (0.43–0.62), and 0.95 (0.79–1.14) for the highest versus lowest tertile of dietary n3, n6 fatty acids intake and n6:n3 ratio, respectively. Dose-response analyses showed that the risk of hypertension was associated with dietary n3 and n6 fatty acids intake. Our study suggested that dietary n3 and n6 fatty acids intake were inversely associated with the risk of hypertension in US adults.

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Long non-coding RNA (lncRNA) H19 has been implicated in tumor angiogenesis. However, whether H19 regulates the progression of corneal neovascularization (CNV) is unclear. The present study aimed to determine the function of H19 in CNV and its possible molecular mechanism. Here, we found that the H19 levels were remarkably increased in vascularized corneas and basic fibroblast growth factor (bFGF)-treated human umbilical vein endothelial cells (HUVECs). In vitro, H19 up-regulation promoted proliferation, migration, tube formation and vascular endothelial growth factor A (VEGFA) expression in HUVECs, and it was found to down-regulate microRNA-29c (miR-29c) expression. Bioinformatics analysis revealed that H19 mediated the above effects by binding directly to miR-29c. In addition, miR-29c expression was markedly reduced in vascularized corneas and its expression also decreased in bFGF-treated HUVECs in vitro. MiR-29c targeted the 3′ untranslated region (3′-UTR) of VEGFA and decreased its expression. These data suggest that H19 can enhance CNV progression by inhibiting miR-29c, which negatively regulates VEGFA. This novel regulatory axis may serve as a potential therapeutic target for CNV.

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