Resveratrol mediates mitochondrial function through the sirtuin 3 pathway to improve abnormal metabolic remodeling in atrial fibrillation.

This study investigated the impact of resveratrol on abnormal metabolic remodeling in atrial fibrillation (AF) and explored potential molecular mechanisms. An AF cell model was established by high-frequency electrical stimulation of HL-1 atrial muscle cells. Resveratrol concentrations were optimized using CCK-8 and flow cytometry. AF-induced increases in ROS and mitochondrial calcium, along with decreased adenosine triphosphate (ATP) and mitochondrial membrane potential, were observed. Resveratrol mitigated these changes and maintained normal mitochondrial morphology. Moreover, resveratrol acted through the SIRT3-dependent pathway, as evidenced by its ability to suppress AF-induced acetylation of key metabolic enzymes. SIRT3 overexpression controls acetylation modifications, suggesting its regulatory role. In conclusion, resveratrol's SIRT3-dependent pathway intervenes in AF-induced mitochondrial dysfunction, presenting a potential therapeutic avenue for AF-related metabolic disorders. This study sheds light on the role of resveratrol in mitigating AF-induced mitochondrial remodeling and highlights its potential as a novel treatment for AF.

Mechanically reinforced biotubes for arterial replacement and arteriovenous grafting inspired by architectural engineering.

There is a lack in clinically-suitable vascular grafts. Biotubes, prepared using in vivo tissue engineering, show potential for vascular regeneration. However, their mechanical strength is typically poor. Inspired by architectural design of steel fiber reinforcement of concrete for tunnel construction, poly(ε-caprolactone) (PCL) fiber skeletons (PSs) were fabricated by melt-spinning and heat treatment. The PSs were subcutaneously embedded to induce the assembly of host cells and extracellular matrix to obtain PS-reinforced biotubes (PBs). Heat-treated medium-fiber-angle PB (hMPB) demonstrated superior performance when evaluated by in vitro mechanical testing and following implantation in rat abdominal artery replacement models. hMPBs were further evaluated in canine peripheral arterial replacement and sheep arteriovenous graft models. Overall, hMPB demonstrated appropriate mechanics, puncture resistance, rapid hemostasis, vascular regeneration, and long-term patency, without incidence of luminal expansion or intimal hyperplasia. These optimized hMPB properties show promise as an alternatives to autologous vessels in clinical applications.

Identifying the key microRNAs implicated in atrial fibrillation.

OBJECTIVE: This study investigated the potential microRNAs (miRNAs) having a diagnostic value in atrial fibrillation (AF). METHODS: The miRNA and mRNA expression profiles of atrial tissue from healthy individuals and patients with AF were downloaded from the Gene Expression Omnibus database. Differentially expressed miRNAs/mRNAs (DEMis/DEMs) were identified in patients with AF. Furthermore, an interaction network between DEMis and DMEs was constructed. The biological processes, molecular functions, and signaling pathways of DEMs were enriched. Then, the diagnostic values of candidate DECs among healthy individuals and patients with AF were preliminarily evaluated in the GSE101586, GSEE101684, and GSE112214 datasets. RESULTS: Twenty DEMis were identified in patients with AF, including seven upregulated and 13 downregulated DEMis. Furthermore, 2,307 DEMs were identified in patients with AF. In the DEMi-DEM interaction network, downregulated miR-193b and upregulated miR-16 interacted with the most targeted DEMs, which interacted with 72 and 65 targeted DEMs, respectively. The targeted DEMs were significantly enriched in biological functions including apoptosis and the PI3K-Akt, mTOR, Hippo, HIF-1, and ErbB signaling pathways. Four of the 20 DEMis (i.e., miR-490-3p, miR-630, miR-146b-5p, and miR-367) had a potential value to distinguish patients with AF from healthy individuals in the GSE68475, GSE70887, and GSE28954 datasets. The area under the curve values for those four DEMis were 0.751, 0.719, 0.709, and 0.7, respectively. CONCLUSION: DEMis might play key roles in AF progression through the mTOR and Hippo signaling pathways. miR-409-3p, miR-630, miR-146b-5p, and miR-367 had a potential diagnostic value to discriminate patients with AF from healthy controls in this study.

Correlation between angiopoietin-like proteins in inflammatory mediators in peripheral blood and severity of coronary arterial lesion in patients with acute myocardial infarction.

The effects of angiopoietin-like protein 2 (Angptl 2) and interleukin-6 (IL-6) in inflammatory mediators on the severity of coronary arterial lesion in patients with acute myocardial infarction were investigated. One hundred and twenty-six patients with acute myocardial infarction admitted to Tianjin Union Medical Center (the myocardial infarction group) and 133 healthy individuals (the control group) were selected for retrospective analysis from January 2013 to December 2015. The levels of Angptl 2 and IL-6 in serum of patients were detected by enzyme linked immunosorbent assay (ELISA), and the correlation analysis between the levels and the degree of coronary stenosis in patients with myocardial infarction was conducted. The expression level of Angptl 2 and IL-6 in the myocardial infarction group was significantly higher than that in the control group P<0.001. In the myocardial infarction group, the expression levels of Angptl 2 and IL-6 were the highest in the patients with severe stenosis, followed by the moderate stenosis, and the lowest in the patients with mild stenosis (P<0.050). Pearson's correlation analysis showed that Angptl 2 and IL-6 were positively correlated with the diameter of coronary stenosis (r=0.696, 0.750, P<0.001). In conclusion, both Angptl 2 and IL-6 are highly expressed in the peripheral blood of patients with acute myocardial infarction and involved in the occurrence and development of the disease. Moreover, Angptl2 and IL-6 are positively correlated with the severity of coronary arterial lesion in patients with acute myocardial infarction, and they are expected to become a target for the diagnosis and treatment of coronary atherosclerosis (CA) in the future.

Identification of Transcription Factor-Gene Regulatory Network in Acute Myocardial Infarction.

BACKGROUND: Acute myocardial infarction (AMI) is a common disease with serious mortality and morbidity, worldwide. The present study aimed to identify differentially expressed genes (DEGs) and construct a transcription factor-gene regulatory network to further study the early diagnosis of AMI. METHODS: The integrated analysis of publicly available Gene Expression Omnibus datasets of AMI was performed. Differentially expressed genes were identified between AMI and normal blood samples. Gene Ontology enrichment analyses, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, and the transcription factor-gene regulatory network were used to obtain insights into the functions of DEGs. Quantitative real-time polymerase chain reactions (qRT-PCR) were performed to validate the expression level of DEGs. RESULTS: A total of 2,502 DEGs, including 917 up-regulated genes and 1,585 down-regulated genes, were identified between AMI and normal blood samples by integrating four expression profiles of AMI. Differentially expressed genes were significantly enriched in pathways including complement and coagulation cascades, Staphylococcus aureus infection, and cell adhesion molecules. Transcription factors were screened and performed to construct the regulatory network. The transcription factor-gene regulatory network consisted of 871 interactions between 80 transcription factors and 716 DEGs. ETS homologous factor (EHF) was one of transcription factors that had high connectivity with DEGs and regulated CACNB4 in the network. Verification by qRT-PCR revealed that EHF, KRT6A and DSG3 were significantly up-regulated, while CACNG4 was significantly down-regulated in AMI. Furthermore, CACNG6, CACNB4 and CLDN18 had a tendency to be down-regulated, and CALML3 had a tendency to be up-regulated in AMI. CONCLUSIONS: The identification of important differentially expressed transcription factors and genes in the development of AMI would be the groundwork for the early diagnosis and early intervention of AMI.

[Involvement characteristics and influencing factors of anxiety and depression in patients after percutaneous coronary intervention].

OBJECTIVE: To explore the involvement characteristics and influencing factors of anxiety and depression in patients after percutaneous coronary intervention (PCI). METHODS: A total of 396 patients undergoing PCI were investigated between January 2009 and December 2010. All of them completed the Hospital Anxiety and Depression Scale (HADS) before discharge and at 12 months post-PCI. We evaluated the involvement characteristics and used Logistic regression to analyze the influencing factors of mood changes. RESULTS: The relevant factors of post-PCI anxiety were gender (P = 0.003), age (P = 0.004) and acute myocardial infarction (P = 0.009) while depression was associated with acute myocardial infarction (P < 0.001). A 12-month follow-up study showed that anxiety remained stable in 76.3% of patients while depression in 79.5%. Multi-factor analysis showed that factors of presence of adverse cardiovascular events (OR: 1.323, 95%CI: 1.026 - 1.705, P = 0.031), Seattle angina score (OR: 0.870, 95%CI: 0.772 - 0.981, P = 0.023) and anxiety scores at pre-discharge (OR: 1.228, 95%CI: 1.053 - 1.432, P = 0.009) were correlated with the deterioration degree of depression. And the factor associated with the deterioration of depression was the scores before discharge (OR: 1.287, 95%CI: 1.072 ∼ 1.545, P = 0.007). CONCLUSION: The levels of anxiety and depression remain stable in the majority of PCI patients at Month 12 post-PCI. Perioperative communication and effective control of postoperative cardiovascular events may ease a patient's negative emotions and improve their living quality.

Coexistence of 2 types of atrial tachycardias and right ventricular outflow tract tachycardia.

Double tachycardia is a relatively uncommon type of tachycardia. In this report, we discuss a 68-year-old woman with history of frequent palpitations. Electrophysiologic study revealed that narrow QRS tachycardias from 2 origins and 1 wide QRS tachycardia were induced and each of the tachycardias was induced by the other. We found that 2 focal atrial tachycardias and 1 ventricular tachycardia originated from right ventricular outflow tract. All of these tachycardias were successfully ablated during one session, and no recurrence appeared during 10 months of follow-up.