a-doxorubicin-induced-murine-model-of-dilated-cardiomyopathy-in-vivo

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Dilated cardiomyopathy (DCM) refers to a spectrum of heterogeneous myocardial disorders characterized by ventricular dilation and depressed cardiac ...

Clinical College of Nanjing Medical University

Patent foramen ovale (PFO) closure has emerged as a secondary prevention option in patients with PFO and cryptogenic stroke. However, the comparative efficacy and safety of percutaneous closure and medical therapy in patients with cryptogenic stroke and PFO remain unclear.

Percutaneous closure versus medical therapy for stroke with patent foramen Ovale: a systematic review and meta-analysis.

The mechanism underlying thrombosis in atrial fibrillation (AF) is not yet clearly understood. The apelin/APJ axis parallel and counter-regulate with the angiotensin system. The present study hypothesizes that apelin/APJ axis exert its anti-thrombus effect in normal left atrial tissue and is disrupted by up-regulated renin-angiotensin-aldosterone system (RAAS) signaling during AF. The specimens of left atrial appendages collected from patients with rheumatic mitral stenosis who underwent valve replacement were divided into 3 groups: sinus rhythm, AF/thrombus, and AF/thrombus. The amounts of angiotensin II receptor subtype 1 (AT1), apelin/APJ and its downstream plasminogen activator inhibitor-1 (PAI-1) were detected by western blot. The expression of apelin/APJ was significantly decreased in the AF/thrombus group compared with the sinus rhythm and AF/thrombus groups. Meanwhile the expressions of AT1 and PAI-1 were highest in the AF/thrombus group compared to the other two groups. Taken together, the present study reveals apelin/APJ axis might be correlated with thrombosis in patients with AF mediated by PAI-1.

Involvement of Apelin/APJ Axis in Thrombogenesis in Valve Heart Disease Patients with Atrial Fibrillation.

Hepatocellular carcinoma (HCC) ranks the third major cause of cancer-associated mortality globally. Numerous studies have attempted to elucidate the underlying mechanisms of HCC using various biomarkers. In the present study, two expression profiles datasets from Gene Expression Omnibus (GSE76427 and GSE84402) and data associated with liver cancer samples from The Cancer Genome Atlas (TCGA) were downloaded for integrated analysis. Five differentially expressed genes (DEGs) exhibiting high expression, including ubiquitin-conjugating enzyme 2C (UBE2C), topoisomerase II α, pituitary tumor transforming gene 1, glypican-3 and polycomb-repressive complex 1, were selected and considered as candidate genes. Enrichment analysis demonstrated that these genes were associated with Gene Ontology terms of cellular components and molecular functions, including regulation of apoptosis, stabilization of p53 and Anaphase Promoting Complex/Cyclosome (APC/C) (APC/C:Cdc20)-mediated degradation of Securin. The expression profiles of these genes in HCC, other human malignancies and different human HCC cell lines were validated using GSE14520, GSE3500 and TCGA data. The results confirmed the upregulation of UBE2C in tissues from patients with HCC or other human malignancies and human liver cancer cell lines, compared with the expression levels in the corresponding adjacent non-tumor tissues and cell lines, respectively. Patients with HCC who exhibited an increased messenger RNA level of UBE2C exhibited a significantly shorter survival time. The results of the present study suggest that the overexpression of UBE2C may be used as a novel prognostic biomarker of HCC.

Identification of the potential therapeutic target gene UBE2C in human hepatocellular carcinoma: An investigation based on GEO and TCGA databases.

The inflammation modulation effects of mesenchymal stromal cell-derived exosomes (MSC-EXO) are well established. We aimed to explore the mechanism behind the inflammatory responses of numerous exosomal cargo molecules that have been neglected in molecular biology research, and to develop an exosomal cargo delivery system that can exert a stronger therapeutic effect on myocardial ischemia-reperfusion (I/R) injury.

miRNA-181a over-expression in mesenchymal stem cell-derived exosomes influenced inflammatory response after myocardial ischemia-reperfusion injury.

Transcatheter aortic-valve replacement (TAVR) has emerged as a promising strategy for treating patients with severe aortic stenosis. We aimed to compare TAVR with surgical aortic-valve replacement (SAVR) and determine the performance of TAVR over time and within several subgroups. We included 8 randomized trials comparing TAVR versus SAVR. Compared with SAVR, TAVR was associated with a lower rate of all-cause mortality or disabling stroke at 30-day (odds ratio [OR], 0.72; p = 0.004), 1-year (OR, 0.83; p = 0.01), and 2-year (OR, 0.86; p = 0.02), but not at long-term follow-up (rate ratio [RR], 1.02 [confidence interval 0.92 to 1.13]; p = 0.67). Notably, 5-year data showed numerically higher incidence in TAVR (RR, 1.11 [confidence interval 0.97 to 1.27]; p = 0.12). The risks associated with TAVR versus SAVR increased over time, showing a significant interaction (p for interaction = 0.01), as were for new-onset atrial fibrillation and rehospitalization. Incidences of major bleeding, new-onset fibrillation, and acute kidney injury were lower in TAVR, whereas transient ischemic attack, major vascular complications, permanent pacemaker implantation, reintervention, and paravalvular leak were lower in SAVR. Incidences for all-cause and cardiovascular mortality, myocardial infarction, and stroke were not statistically different. TAVR with transfemoral approach and new-generation valve was associated with reduction in all-cause mortality or disabling stroke compared with corresponding comparators. In conclusion, TAVR was associated with a lower risk for all-cause mortality or disabling stroke within 2 years, but not at long-term follow-up compared with SAVR; the risks seems to increase over time. More data are needed to determine longer-term performance of TAVR.

Meta-Analysis Comparing Results of Transcatheter Versus Surgical Aortic-Valve Replacement in Patients With Severe Aortic Stenosis.

Dilated cardiomyopathy (DCM) is one of the leading causes of heart failure. A large proportion of genetic cause remains unexplained, especially in idiopathic DCM. We performed target next-generation sequencing of 102 genes which were known causes or candidate genes for cardiomyopathies and channelpathies in 118 prospectively recruited Han Chinese patients with idiopathic DCM. 41 of the 118 patients carried 40 pathogenic or likely pathogenic variants, providing a molecular diagnosis in 34.7% of patients. 32 of these variants were novel. TTN truncating variants were predominant, with a frequency of 31.0%, followed by variants of LMNA (14.3%), RBM20 (4.8%), and NEXN (4.8%). These 4 genes accounted for over half variants identified. No significant difference in clinical characteristics or rates of reaching the composite end point (cardiac transplantation and death from cardiac causes) between pathogenic or likely pathogenic variant carriers and noncarriers (hazard ratio 1.11, 95% CI: 0.41 to 3.00), or between patients with TTN truncating variants or without (hazard ratio 0.49, 95% CI: 0.36 to 6.10). In our prospective study, we first determined the overall genetic profiles and genotype-phenotype correlations in Han Chinese idiopathic DCM patients, which could provide insight for genetic diagnosis of DCM in this population.

Genetic Basis and Genotype-Phenotype Correlations in Han Chinese Patients with Idiopathic Dilated Cardiomyopathy.

The cardiac repair after myocardial infarction (MI) involves two phases, namely, inflammatory response and proliferative response. The former is an inflammatory reaction, evoked by different kinds of pro-inflammatory leukocytes and molecules stimulated by myocardial necrosis, while the latter is a repair process, predominated by a magnitude of anti-inflammatory cells and cytokines, as well as fibroblasts. Cardiac remodeling post-MI is dependent on the balance of individualized intensity of the post-MI inflammation and subsequent cardiac fibrosis. During the past 30 years, enormous studies have focused on investigating immune cells and mediators involved in cardiac inflammation and fibrosis, which are two interacting processes of post-MI cardiac repair. These results contribute to revealing the mechanism of adverse cardiac remodeling after MI and alleviating the impairment of cardiac function. In this study, we will broadly discuss the role of immune cell subpopulation and the involved cytokines and chemokines during cardiac repair post-MI, particular in cardiac inflammation and fibrosis.

Biao Xu

Department of Cardiology,
Nanjing Drum Tower Hospital,
Department of Cardiology, Nanjing Drum Tower Hospital

Clinical College of Nanjing Medical University

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Biao Xu

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Department of Cardiology,Nanjing Drum Tower Hospital,Department of Cardiology, Nanjing Drum Tower Hospital

Clinical College of Nanjing Medical University

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo

Department of Cardiology,
Nanjing Drum Tower Hospital,
Department of Cardiology, Nanjing Drum Tower Hospital