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Background Calcific aortic valve disease (CAVD) is a common valve disease with an increasing incidence, but no effective drugs as of yet. With the development of sequencing technology, non-coding RNAs have been found to play roles in many diseases as well as CAVD, but no circRNA/lncRNA–miRNA–mRNA interaction axis has been established. Moreover, valve interstitial cells (VICs) and valvular endothelial cells (VECs) play important roles in CAVD, and CAVD differed between leaflet phenotypes and genders. This work aims to explore the mechanism of circRNA/lncRNA–miRNA–mRNA network in CAVD, and perform subgroup analysis on the important characteristics of CAVD, such as key cells, leaflet phenotypes and genders. Results We identified 158 differentially expressed circRNAs (DEcircRNAs), 397 DElncRNAs, 45 DEmiRNAs and 167 DEmRNAs, and constructed a hsa-circ-0073813/hsa-circ-0027587–hsa-miR-525-5p–SPP1/HMOX1/CD28 network in CAVD after qRT-PCR verification. Additionally, 17 differentially expressed genes (DEGs) in VICs, 9 DEGs in VECs, 7 DEGs between different leaflet phenotypes and 24 DEGs between different genders were identified. Enrichment analysis suggested the potentially important pathways in inflammation and fibro-calcification during the pathogenesis of CAVD, and immune cell patterns in CAVD suggest that M0 macrophages and memory B cells memory were significantly increased, and many genes in immune cells were also differently expressed. Conclusions The circRNA/lncRNA–miRNA–mRNA interaction axis constructed in this work and the DEGs identified between different characteristics of CAVD provide a direction for a deeper understanding of CAVD and provide possible diagnostic markers and treatment targets for CAVD in the future.

Myocardial infarction results from obstruction of a coronary artery that causes insufficient blood supply to the myocardium and leads to ischemic necrosis. It is one of the most common diseases threatening human health and is characterized by high morbidity and mortality. Atherosclerosis is the pathological basis of myocardial infarction, and its pathogenesis has not been fully elucidated. Innate lymphoid cells (ILCs) are an important part of the human immune system and participate in many processes, including inflammation, metabolism and tissue remodeling, and play an important role in atherosclerosis. However, their specific roles in myocardial infarction are unclear. This review describes the current understanding of the relationship between innate lymphoid cells and myocardial infarction during the acute phase of myocardial infarction, myocardial ischemia-reperfusion injury, and heart repair and regeneration following myocardial infarction. We suggest that this review may provide new potential intervention targets and ideas for treatment and prevention of myocardial infarction.

According to some recent observational studies, the gut microbiota influences atherosclerosis via the gut microbiota-artery axis. However, the causal role of the gut microbiota in atherosclerosis remains unclear. Therefore, we used a Mendelian randomization (MR) strategy to try to dissect this causative link. The biggest known genome-wide association study (GWAS) (n = 13,266) from the MiBioGen collaboration was used to provide summary data on the gut microbiota for a two-sample MR research. Data on atherosclerosis were obtained from publicly available GWAS data from the FinnGen consortium, including cerebral atherosclerosis (104 cases and 218,688 controls), coronary atherosclerosis (23,363 cases and 187,840 controls), and peripheral atherosclerosis (6631 cases and 162,201 controls). The causal link between gut microbiota and atherosclerosis was investigated using inverse variance weighting, MR-Egger, weighted median, weighted mode, and simple mode approaches, among which inverse variance weighting was the main research method. Cochran's Q statistic was used to quantify the heterogeneity of instrumental variables (IVs), and the MR Egger intercept test was used to assess the pleiotropy of IVs. Inverse-variance-weighted (IVW) estimation showed that had a protective influence on cerebral atherosclerosis (OR = 0.10, 95% CI: 0.01-0.67, = 0.018), while (OR = 5.39, 95% CI: 1.50-19.37, = 0.010), (OR = 6.87, 95% CI: 1.60-29.49, = 0.010), (OR = 2.88, 95% CI: 1.18-7.05, = 0.021), and (OR = 5.26, 95% CI: 1.28-21.61, = 0.021) had pathogenic effects on cerebral atherosclerosis. For (OR = 0.87, 95% CI: 0.76-0.99, = 0.039), the (OR = 0.89, 95% CI: 0.80-1.00, = 0.048), the (OR = 0.80, 95% CI: 0.69-0.94, = 0.006), and the (OR = 0.87, 95% CI: 0.77-0.98, = 0.023) were protective against coronary atherosclerosis. However, the (OR = 1.12, 95% CI: 1.00-1.24, = 0.049) had a pathogenic effect on coronary atherosclerosis. Finally, (OR = 0.83, 95% CI: 0.69-0.99, = 0.036), (OR = 0.76, 95% CI: 0.61-0.94, = 0.013), (OR = 0.76, 95% CI: 0.60-0.96, = 0.022), and (OR = 0.65, 95% CI: 0.46-0.92, = 0.013), these four microbiota have a protective effect on peripheral atherosclerosis. However, for the (OR = 1.25, 95% CI: 1.01-1.56, = 0.040) and the (OR = 1.22, 95% CI: 1.04-1.42, = 0.016), there is a pathogenic role for peripheral atherosclerosis. No heterogeneity was found for instrumental variables, and no considerable horizontal pleiotropy was observed. We discovered that the presence of probiotics and pathogens in the host is causally associated with atherosclerosis, and atherosclerosis at different sites is causally linked to specific gut microbiota. The specific gut microbiota associated with atherosclerosis identified by Mendelian randomization studies provides precise clinical targets for the treatment of atherosclerosis. In the future, we can further examine the gut microbiota's therapeutic potential for atherosclerosis if we have a better grasp of the causal relationship between it and atherosclerosis.

Until now, few articles have revealed the potential roles of innate lymphoid cells (ILCs) in cardiovascular diseases. However, the infiltration of ILC subsets in ischemic myocardium, the roles of ILC subsets in myocardial infarction (MI) and myocardial ischemia-reperfusion injury (MIRI) and the related cellular and molecular mechanisms have not been described with a sufficient level of detail. In the current study, 8-week-old male C57BL/6J mice were divided into three groups: MI, MIRI and sham group. Single-cell sequencing technology was used to perform dimensionality reduction clustering of ILC to analyze the ILC subset landscape at a single-cell resolution, and finally flow cytometry was used to confirm the existence of the new ILC subsets in different disease groups. Five ILC subsets were found, including ILC1, ILC2a, ILC2b, ILCdc and ILCt. It is worth noting that ILCdc, ILC2b and ILCt were identified as new ILC subclusters in the heart. The cellular landscapes of ILCs were revealed and signal pathways were predicted. Furthermore, pseudotime trajectory analysis exhibited different ILC statuses and traced related gene expression in normal and ischemic conditions. In addition, we established a ligand-receptor-transcription factor-target gene regulatory network to disclose cell communications among ILC clusters. Moreover, we further revealed the transcriptional features of the ILCdc and ILC2a subsets. Finally, the existence of ILCdc was confirmed by flow cytometry. Collectively, by characterizing the spectrums of ILC subclusters, our results provide a new blueprint for understanding ILC subclusters' roles in myocardial ischemia diseases and further potential treatment targets.

Cardiovascular disease (CVD) remains the leading cause of mortality globally. Circular RNAs (circRNAs) have attracted extensive attention for their roles in the physiological and pathological processes of various cardiovascular diseases (CVDs). In this review, we briefly describe the current understanding of circRNA biogenesis and functions and summarize recent significant findings regarding the roles of circRNAs in CVDs. These results provide a new theoretical basis for diagnosing and treating CVDs.

Calciphylaxis, also termed calcific uremic arteriolopathy (CUA) in patients with end-stage kidney disease (ESKD), is a rare and fatal condition characterized by cutaneous ischemic necrosis. Three patients with calciphylaxis and metastatic pulmonary calcification (MPC) were treated with human amnion-derived mesenchymal stem cells (hAMSCs). Effects were evaluated using the Visual Analogue Scale (VAS), modified Bates-Jensen Wound Assessment Tool for CUA (BWAT-CUA), wound quality of life questionnaire (Wound-QoL), and histological analysis. MPC was assessed by high-resolution CT (HRCT) and ᵐTc-methylene diphosphonate ( ᵐTc-MDP) bone scans. ᵐTc-labeled macroaggregated albumin ( ᵐTc-MAA) pulmonary perfusion imaging was conducted for the first time in patients with MPC. Three patients exhibited wound healing and improvement in skin symptoms. Two months before CUA, asymptomatic MPC was detected in Patient 1, who was treated with hAMSCs for 15 months. The condition progressed to chest pain and dyspnea. HRCT and ᵐTc-MDP bone scans showed worsening calcification, particularly in the upper and mid-thoracic lobes. ᵐTc-MAA pulmonary perfusion imaging revealed impaired or absent blood perfusion in the areas of metastatic calcification. Patient 1 died from respiratory failure. Patients 2 and 3 had asymptomatic MPC at calciphylaxis diagnosis. After 2 months of treatment, Patient 2, showed no significant imaging improvement and passed away 6 months after discontinuing hAMSC treatment. Patient 3 has shown no significant progression of pulmonary lesions and continues hAMSC therapy. We reported personalized early, noninvasive diagnosis and regenerative treatments for calciphylaxis patients with MPC. Although the current hAMSC treatment regimen is effective for skin lesions, its impact on MPC requires further investigation.

Purpose The purpose of this paper is to analyse the factors that influence food safety reporting intention and behaviour of the public. Design/methodology/approach Data used in this study came from a questionnaire survey conducted in Shandong Province, China. The 642 qualified samples were analysed through structural equation model based on the expanded theory of planned behaviour to study public food safety reporting behaviour and its influencing factors. Findings Results indicated that participation attitude, subjective norm, perceived behavioural control (PBC) and moral norm had significantly positive effects on public reporting intention, which had a direct effect on behaviour. Among subjective norm, descriptive norm had a more significant influence on the intention to report than injunctive norm. PBC indirectly affected reporting behaviour through participation intention, and directly affected participation behaviour. Socio-demographic variables had significant influence on participation attitude, injunctive norm and PBC, whereas these variables had no influence on descriptive norm and moral norm. Originality/value This research is of academic value and of value to policy makers. To promote public participation in food safety reporting, the government should consider influencing factors of food safety reporting.

Purpose - The purpose of this paper is to classify and identify the acoustic emission (AE) signals of 304 stainless steel during stress corrosion process.Design methodology approach - The corrosion behavior of a specimen during slow strain rate testing (SSRT) in acidic NaCl solution was studied. The AE signals during the corrosion process were classified based on K-means cluster algorithms; meanwhile, the characteristics of different AE sources were analyzed.Findings - The results indicated that the AE characteristics of different AE sources, such as pitting, cracking, and bubble break-up, differ significantly. The 304 stainless steel was prone to the occurrence of stress corrosion cracking under the SSRT condition in acidic NaCl solution.Originality value - The characteristics of different AE sources during corrosion process were gained for the first time, which could be of much help in analyzing and judging the corrosion situation.