Correlation between serum uric acid to high-density lipoprotein cholesterol ratio and atrial fibrillation in patients with NAFLD.

Background: Non-alcoholic fatty liver disease (NAFLD) is independently associated with atrial fibrillation (AF) risk. The uric acid (UA) to high-density lipoprotein cholesterol (HDL-C) ratio (UHR) has been shown to be closely associated with cardiovascular disease (CVD) and NAFLD. The aim of this study is to clarify whether elevated UHR is associated with the occurrence of AF in patients with NAFLD and to determine whether UHR predicted AF.

C1q/Tumor Necrosis Factor-Related Protein-9 Enhances Macrophage Cholesterol Efflux and Improves Reverse Cholesterol Transport via AMPK Activation.

Cholesterol efflux from foam cells in atherosclerotic plaques is crucial for reverse cholesterol transport (RCT), an important antiatherogenic event. ATP-binding cassette (ABC) transporters, ABCA1 and ABCG1, are key receptors in the cholesterol efflux pathway. C1q/tumor necrosis factor-related protein-9 (CTRP9) is a newly discovered adipokine and exhibits an atheroprotective activity.

The neutrophil-to-lymphocyte ratio is a potential biomarker for the occurrence of atrial fibrillation in patients with obstructive sleep apnea: A BIOMARKER OF AF IN OSA PATIENTS.

Background: Obstructive sleep apnea (OSA) affects the occurrence of atrial fibrillation (AF) and usually coexists with AF. Chronic inflammation has been identified as an important factor in the development of AF, and the neutrophil-to-lymphocyte ratio (NLR) has been identified as a biomarker that positively correlates with the degree of inflammation. However, little information regarding how NLR correlates with AF in OSA patients.

Circulating Th17/Treg as a promising biomarker for patients with rheumatoid arthritis in indicating comorbidity with atherosclerotic cardiovascular disease.

Background: Immune and inflammatory responses have a pivotal role in the pathogenesis of rheumatoid arthritis (RA) and atherosclerotic cardiovascular disease (ASCVD). This study aims to explore the change of peripheral lymphocytes, especially the absolute and relative changes in peripheral T cells in RA patients with and without ASCVD.

Hypothesis: The changes in the lymphocyte subsets were assessed to provide a novel insight in diagnosing and preventing ASCVD in patients with RA.

Chronic intermittent hypoxia-induced BNIP3 expression mitigates contractile dysfunction and myocardial injury in animal and cell model via modulating autophagy.

Obstructive sleep apnea syndrome is generally associated with multiple cardiovascular disorders, such as myocardial hypertrophy. Autophagy is strictly modulated to maintain cardiac homeostasis. Post-injury autophagy is closely associated with pathological cardiac hypertrophy.

Activating transcription factor 3 is a potential target and a new biomarker for the prognosis of atherosclerosis.

ATF3 (activating transcription factor 3) is a member of the mammalian activation transcription factor/cAMP-responsive element-binding (CREB) family. It plays a role in inflammation and innate immunity, and suggests that ATF3 is associated with atherosclerosis. In our study, we analyzed datasets of atherosclerosis from the NCBI-GEO (Gene Expression Omnibus) database and found that expression levels of ATF3 were lower in macrophages from ruptured atherosclerotic plaques than from stable atherosclerotic plaques.

P‑selectin increases angiotensin II‑induced cardiac inflammation and fibrosis via platelet activation.

Platelet activation is important in hypertension‑induced cardiac inflammation and fibrosis. P-selectin expression significantly (P<0.05) increases when platelets are activated during hypertension.

High glucose/High Lipids impair vascular adiponectin function via inhibition of caveolin-1/AdipoR1 signalsome formation.

Reduced levels of adiponectin (APN) contribute to cardiovascular injury in the diabetic population. Recent studies demonstrate elevated circulating APN levels are associated with endothelial dysfunction during pre-diabetes, suggesting the development of APN resistance. However, mechanisms leading to, and the role of, vascular APN resistance in endothelial dysfunction remain unidentified.

RNA interference targeting the ACE gene reduced blood pressure and improved myocardial remodelling in SHRs.

The purpose of the present study was to investigate the effects on blood pressure and myocardial hypertrophy in SHRs (spontaneously hypertensive rats) of RNAi (RNA interference) targeting ACE (angiotensin-converting enzyme). SHRs were treated with normal saline as vehicle controls, with Ad5-EGFP as vector controls, and with recombinant adenoviral vectors Ad5-EGFP-ACE-shRNA, carrying shRNA (small hairpin RNA) for ACE as ACE-RNAi. WKY (Wistar-Kyoto) rats were used as normotensive controls treated with normal saline.