Chronic thromboembolic pulmonary hypertension (CTEPH) is one of the primary causes of severe pulmonary hypertension. In order to identify long noncoding RNAs (lncRNAs) that may be involved in the development of CTEPH, comprehensive lncRNA and messenger RNA (mRNA) profiling of endothelial tissues from the pulmonary arteries of CTEPH patients was conducted with microarray analysis. Differential expression of 185 lncRNAs was observed in the CTEPH tissues compared with healthy control tissues. Further analysis identified 464 regulated enhancer‑like lncRNAs and overlapping, antisense or nearby mRNA pairs. Coexpression networks were subsequently constructed and investigated. The expression levels of the lncRNAs, NR_036693, NR_027783, NR_033766 and NR_001284, were significantly altered. Gene ontology and pathway analysis demonstrated the potential role of lncRNAs in the regulation of central process, including inflammatory response, response to endogenous stimulus and antigen processing and presentation. The use of bioinformatics may help to uncover and analyze large quantities of data identified by microarray analyses, through rigorous experimental planning, statistical analysis and the collection of more comprehensive data regarding CTEPH. The results of the present study provided evidence which may be helpful in future studies on the diagnosis and management of CTEPH.

Coronary artery disease (CAD) is a prevalent cardiovascular condition, and numerous studies have linked gut bacterial imbalance to CAD. However, the relationship of gut fungi, another essential component of the intestinal microbiota, with CAD remains poorly understood. In this cross-sectional study, we analyzed fecal samples from 132 participants, split into 31 healthy controls and 101 CAD patients, further categorized into stable CAD (38), unstable angina (41), and acute myocardial infarction (22) groups. We conducted internal transcribed spacer 1 (ITS1) and 16S sequencing to examine gut fungal and bacterial communities. Based on ITS1 analyses, Ascomycota and Basidiomycota were the dominant fungal phyla in all the groups. The α diversity of gut mycobiome remained unaltered among the control group and CAD subgroups; however, the structure and composition of the mycobiota differed significantly with the progression of CAD. The abundances of 15 taxa gradually changed with the occurrence and progression of the disease and were significantly correlated with major CAD risk factor indicators. The mycobiome changes were closely linked to gut microbiome dysbiosis in patients with CAD. Furthermore, disease classifiers based on gut fungi effectively identified subgroups with different degrees of CAD. Finally, the FUNGuild analysis further categorized these fungi into distinct ecological guilds. In conclusion, the structure and composition of the gut fungal community differed from healthy controls to various subtypes of CAD, revealing key fungi taxa alterations linked to the onset and progression of CAD. Our study highlights the potential role of gut fungi in CAD and may facilitate the development of novel biomarkers and therapeutic targets for CAD. This work was supported by the grants from the National Natural Science Foundation of China (No. 82170302, 92168117, 82370432), National clinical key specialty construction project- Cardiovascular Surgery, the Reform and Development Program of Beijing Institute of Respiratory Medicine (No. Ggyfz202417, Ggyfz202308), the Beijing Natural Science Foundation (No. 7222068); and the Clinical Research Incubation Program of Beijing Chaoyang Hospital Affiliated to Capital Medical University (No. CYFH202209).

Atrial fibrillation (AF) is a highly heterogeneous genetic disease; however, the pathogenesis of AF cannot be explained by genetic variants alone. DNA methylation is a heritable method of gene expression regulation, and may be a potential regulatory mechanism in AF. Therefore, in the present study, the genome-wide DNA methylation pattern in cells derived from the left atrium of patients with permanent AF (n=7) was compared with that of healthy heart donors (n=4) with a normal sinus rhythm (SR). Enriched biological functions of the differentially methylated genes were assessed. Integrated analysis of genome-wide methylation and mRNA expression profiles was performed, and reverse transcription quantitative-polymerase chain reaction (RT-qPCR) was used to determine the expression levels of four selected genes. A total of 417 differentially methylated CpG sites were identified in the fibrillating atrium (P0.17); the majority of which were located in gene-body and intergenic regions outside of CpG islands. Aberrantly methylated genes participated in the activation of inflammation, sodium and potassium ion transport, fibrosis and the reduction of lipid metabolism. Hypermethylation in the AF susceptible loci, paired-like homeodomain transcription factor 2 (chromosome 4q25) and coiled-coil domain containing 141 (chromosome 2q31), as well as hypomethylation in the calcium voltage-gated channel subunit alpha 1C (chromosome 12p13) locus, were identified in all patients with AF. Of the 420 upregulated and 567 downregulated genes previously identified in patients with AF relative to those with normal SR (fold-change >2.0; P <= 0.05), 12 genes were hypomethylated and eight genes were hypermethylated in each group, respectively (vertical bar beta vertical bar>0.2: P<0.05). RT-qPCR analysis of four of these genes supported the modulatory effect of DNA methylation on gene expression. These results suggest that DNA methylation-mediated regulation of gene expression may serve an important role in AF pathogenesis, and several susceptible AF CpG loci were identified which may be involved in the initiation of AF.

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and is associated with increased risks of stroke and heart failure. However, the exact mechanisms of left atrium remodeling and AF-related biological behaviors are not completely understood. The transcripts of left atrium in permanent atrium fibrillation patients (n = 7) were compared with those of healthy heart donors (n = 4) in sinus rhythm using Agilent 4x44K microarrays. Differently expressed genes were analyzed based on Gene Ontology and KEGG and Biocarta pathway analysis databases. We identified 567 down- and 420 up-regulated genes in atrial fibrillation. The majority of the down-regulated genes participated in metabolic processes, particularly that for fatty acids. The most remarkable up-regulating effects were immune and platelet activation. In addition, atrial remodeling including structural, contractile, electrophysiological, neurohormone, and oxidant stress was also observed, suggesting various pathophysiology changes in fi brillating atrium. Nine AF closely related genes were validated by real-time RT-PCR. Some AF specific genes were determined which may be a complement to the mechanism of left atrium remodeling. Metabolic changes and inflammation could promote or aggravate atrial fibrillation.

Background: The relationship between body mass index (BMI) and low-density lipoprotein cholesterol (LDL-C) has not been clearly elucidated in middle-aged and older adults. This study aimed to evaluate the non-linear dose-response relationship between BMI and LDL-C in males and females. Methods: Data was obtained from two nationally representative surveys in China—the China Health and Nutrition Survey (CHNS, 2009) and China Health and Retirement Longitudinal Study (CHARLS, 2011–2012). To evaluate the sex differences in the association between BMI and LDL-C, the generalized additive models with a smooth function for continuous BMI and smooth-factor interaction for sexes with BMI were used. Segmented regressions were fitted to calculate the slopes with different estimated breakpoints among females and males. Results: A total of 12,273 participants (47.1% male) aged 45 to 75 years were included. The generalized additive models revealed that a non-linear relationship between BMI and LDL-C level in both sexes after adjustment for age, residence, education levels, marital status, drinking, smoking status, and cohort (CHNS or CHARLS). Slopes of the association between BMI and LDL-C association changed at BMI 20.3 kg/m² (95% CI: 18.8 to 21.8) in females and 27.1 kg/m² (95% CI: 25. 8 to 28.4) in males. Below these BMI breakpoints, LDL-C levels increased 1.84 (95% CI: 1.45 to 2.31) in males and 3.49 (95% CI: 1.54 to 5.45) mg/dL per kg/m² in females. However, LDL-C levels declined − 1.50 (95% CI: − 2.92 to − 0.09) mg/dL per kg/m² above BMI of 27.1 kg/m² in males. The non-linear association BMI and LDL-C in males and females was varied by cohort source, age groups, and the number of metabolic syndrome criteria. Conclusions: In the Chinese middle aged and older adults, the BMI and LDL-C relationship was inverted U-shaped with a high level of LDL-C at a BMI of 27.1 kg/m² in males, and an approximately linear association was observed in females.