Association between hypertension and the prevalence of liver steatosis and fibrosis.

BACKGROUND: Hypertension (HTN) and non-alcoholic fatty liver disease (NAFLD) frequently coexist and share pathophysiological symptoms. Based on the liver stiffness measurement and controlled attenuation parameter obtained by performing liver transient ultrasound elastography (TUE), we determined the relationship between HTN status and the rates of liver steatosis and fibrosis in this study. METHODS: To perform this cross-sectional study, data were obtained from the National Health and Nutrition Examination Survey for 2017-March 2020 Pre-pandemic cycle. The relationship between HTN and the rates of liver steatosis and fibrosis was analyzed by constructing a multivariate logistic regression model. The VCTE was performed using a FibroScan® system (model 502, V2 Touch), and CAP was measured at ≥ 274 dB/m for liver steatosis, and the LSM result (median, ≥ 8 kPa) confirmed fibrosis. We also conducted subgroup analyses based on the age, sex, ethnicity, and body mass index (BMI) of the patients. RESULTS: In total, 4,705 participants were recruited, including 2,287 participants with HTN and 2,418 without HTN. After adjusting possible confounders, HTN was positively related to the liver steatosis rate (OR = 1.4, 95% CI: 1.1-1.8). Such HTN-associated prevalence was higher among males (OR = 1.6, 95% CI: 1.1-2.2), non-Hispanic African American individuals (OR = 2.1, 95% CI: 1.1-3.7), and participants with BMI ≥ 25 < 30 kg/m2 (OR = 1.7, 95% CI: 1.1-2.5). Additionally, HTN was positively associated with the fibrosis rate (OR = 2.0, 95% CI: 1.3-3.0), especially among females (OR = 2.6, 95% CI: 1.3-5.2), among individuals who were 40-59 years old (OR = 2.1, 95% CI: 1.0-4.3), 60-80 years old (OR = 2.4, 95% CI:1.3-4.6), non-Hispanic Caucasian (OR = 2.9, 95% CI: 1.5-5.6), among those with BMI ≥ 25 < 30 kg/m2 (OR = 3.0, 95% CI: 1.1-8.2), and those with BMI ≥ 30 kg/m2 (OR = 2.1, 95% CI: 1.4-3.2). CONCLUSION: The results of this study revealed that HTN status was associated with higher rates of liver steatosis and fibrosis, particularly in subjects with BMI ≥ 25 kg/m2. The ethnicity of the participants also had an impact on the relationship.

QishenYiqi dripping pill protects against myocardial ischemia/reperfusion injury via suppressing excessive autophagy and NLRP3 inflammasome based on network pharmacology and experimental pharmacology.

Background: Myocardial ischemia/reperfusion (I/R) injury is associated with multiple serious clinical manifestations. Autophagy is upregulated in a short period of ischemia and further enhanced during reperfusion phase, which was considered as a "double-edged sword" in the pathological process of myocardial I/R injury. In addition, NLRP3 inflammasome triggers myocardial inflammatory response, which leads to cardiomyocyte death via pyroptosis and promotes subsequent myocardial remodelling. Qishen Yiqi Dripping Pill (QSYQ) has been recognized as a potential protective agent of cardiovascular diseases. Objective: We predicted the bioactive compounds, targets and pathways of OSYQ intervening on myocardial I/R injury by network pharmacology. Furthermore, we investigated the effect of QSYQ on myocardial I/R injury and explored its underlying mechanism via autophagy and NLRP3 Inflammasome. Methods: Bioactive compounds, targets of QSYQ and relevant targets of myocardial I/R injury were collected from public databases. The protein-protein interaction network, Gene ontology and KEGG pathway enrichment analysis were carried out to screen the key compounds, target genes, functional annotation and pivotal pathways. Molecular docking was used to validate the binding association between target genes and key bioactive ingredients. Furthermore, sixty SD rats were randomized into four groups: 1) sham, 2) model, 3) captopril and 4) QSYQ pretreatment (14 days before and after surgery). Each arm was subjected to ischemia/reperfusion surgery except sham arm (30 min coronary ligation, then reperfusion). Left ventricular (LV) function were evaluated and the hearts were used to evaluate size of myocardial infarction, cardiomyocyte fibrosis, and myocardial autophagosomes. Results: The network pharmacology revealed the mechanism of QSYQ intervening on myocardial I/R injury might be related to NOD-like receptor signaling pathway, PI3K-Akt signaling pathway, autophagy-animal, etc., Molecular-docking suggested the core target proteins had good binding association with bioactive compounds of QSYQ. The experiment confirmed that QSYQ attenuated myocardial infarct size, decreased inflammatory infiltration and collagen fiber deposition and alleviated the autophagosome and myocardium ultrastructure injury, leading to LV systolic function improvement. The possible mechanism of cardioprotection was due to regulating autophagy-related proteins, activating PI3K/Akt-mTOR signaling pathway, and inhibiting activation and assembly of NLRP3 inflammasome. Conclusion: QSYQ ameliorated myocardial I/R injury via suppressing excessive autophagy and NLRP3 Inflammasome.

Targeting Epigenetics and Non-coding RNAs in Myocardial Infarction: From Mechanisms to Therapeutics.

Myocardial infarction (MI) is a complicated pathology triggered by numerous environmental and genetic factors. Understanding the effect of epigenetic regulation mechanisms on the cardiovascular disease would advance the field and promote prophylactic methods targeting epigenetic mechanisms. Genetic screening guides individualised MI therapies and surveillance. The present review reported the latest development on the epigenetic regulation of MI in terms of DNA methylation, histone modifications, and microRNA-dependent MI mechanisms and the novel therapies based on epigenetics.