Whole blood transcriptomic profiling in men and women with heart failure
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE181114 | GEO | 2023/03/01
REPOSITORIES: GEO
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Project description:Whole blood transcriptomic profiling in men and women with heart failure
| PRJNA750774 | ENA
Project description:Inflammatory mediators play a role in the pathogenesis/progression of chronic heart failure (CHF). The aim of the present study was to identify diagnostic/prognostic markers and gene expression profiles of CHF vs control. Keywords: CHF patients profiling vs controls.
2007-09-22 | GSE9128 | GEO
Project description:Background: Chronic heart failure (CHF) is a major public health problem with high mortality and morbidity worldwide. Shexiang Tongxin Dropping Pill (STDP) is a widely used traditional Chinese medicine preparation for coronary heart disease and growing evidence proves that STDP exerts beneficial effects on CHF in the clinic. However, the mechanism of its effect on CHF still yet to be deciphered. Objective: This study aimed to elucidate the potential pharmacological mechanism of STDP against CHF by integrating network pharmacology analysis and whole-transcriptome sequencing. Methods: First, the mouse model of CHF was established by the transverse aortic constriction (TAC) surgery, and the efficacy of STDP against CHF was evaluated by assessing the alterations in cardiac function, myocardial fibrosis, and cardiomyocyte hypertrophy with echocardiography, Masson's trichrome staining, and wheat germ agglutinin staining. Next, a CHF disease network was constructed by integrating cardiovascular disease-related genes and the transcriptome sequencing data of mouse heart tissue, which was used to explore the underlying mechanism of action of STDP in CHF. Then, the key targets involved in the effects of STDP on CFH were determined by network analysis algorithms, and pathway enrichment analysis was performed to these key genes. Finally, important targets in the critical pathway were verified in vivo. Results: STDP administration (86 mg/kg/d) obviously improved cardiac function, relieved cardiomyocyte hypertrophy, and ameliorated myocardial fibrosis in CFH mice. Moreover, STDP significantly reversed the imbalanced genes that belong to the disease network of CHF in mice with TAC, and the number of genes with the reverse effect was 395. Pathway analysis of the crucial genes with recovery efficiency revealed that pathways related to fibrosis and energy metabolism were highly enriched, while TGF-β pathway and ERK/MAPK pathway were predicted to be significantly affected. Consistently, validation experiments confirmed that inhibiting ERK/MAPK and TGF-β signaling pathways via reduction of the phosphorylation level of Samd3 and ERK1/2 is the important mechanism of STDP against CHF. Conclusion: Our data provided strong evidence that STDP has great potential for the treatment of CHF and the mechanisms are mainly related to inhibition of ERK/MAPK and TGF-β signaling pathways.
2021-10-27 | GSE185631 | GEO
Project description:In chronic heart failure (CHF), functional and metabolic alterations are detected not only in cardiac muscle but also in skeletal muscle tissue. The molecular mechanisms responsible for muscle dysfunction in patients with CHF remain unknown as well as the biological processes responsible for the positive effect of physical exercise training. In this work, using the results of transcriptome sequencing (3' mRNA-Seq), authors identify the molecular mechanisms responsible for reducing muscle dysfunctions in patients with CHF undergoing a personalized program of physical rehabilitation. 3 patients with CHF were enrolled in the study, biopsies of gastrocnemius muscle were taken before and after 12 weeks of individual training program (intensity was determined at 90% of lactate inflection point). Analysis of RNA-Seq data shows the strong upregulation of pathways that control skeletal muscle cell differentiation, muscle contraction, recovery of membrane potential.
2019-12-04 | GSE134698 | GEO
Project description:Particulate Matter Triggers Carotid Body Dysfunction, Respiratory Dysynchrony and Cardiac Arrhythmias in Mice with Cardiac Failure; The mechanistic link between human exposure to airborne particulate matter (PM) pollution and the increased cardiovascular morbidity and mortality observed in people with congestive heart failure (CHF) is unknown. We now show that exposure of genetically-engineered mice with CHF (expressing a cardiac-specific CREB mutant transcription factor) to ambient PM (collected in Baltimore, mean aerodynamic diameter 1.9 um) unmasks severe autonomic morbidities manifested as significant reductions in heart rate variability, respiratory dysynchrony and increased frequency of serious ventricular arrhythmias, features not observed in PM-challenged wild type mice without CHF. PM exposure in CREB mice with CHF reflexly triggers autonomic dysfunction via heightened carotid body function as evidenced by pronounced afferent nerve responses to hypoxia and marked depression of breathing by hyperoxia challenge. Genomic analyses of lung and ventricular tissues revealed PM-induced molecular signatures of inflammation and oxidative stress. These findings in a murine model of cardiac failure provide the first direct assessment of autonomic function in response to PM challenge and are highly consistent with current epidemiologic findings on cardiovascular morbidity in susceptible PM-exposed human populations. We utilized a murine model of dilated cardiomyopathy to address potential mechanistic links between PM exposure and the development of life-threatening cardiac dysrhythmias. Experiment Overall Design: four group (n=3) of animals were treated by PBS or particulate matter (20mg/kg 1.9µm particulate matter) in Wild type or CD-1 dominate negative mice
2009-08-15 | E-GEOD-17478 | biostudies-arrayexpress
Project description:In this study, we aimed to identify novel serum biomarkers in feline primary cardiomyopathies with congestive heart failure, which can help to understand disease pathogenesis and assist the disease diagnosis, prognosis and management. The study included 15 cats diagnosed with CHF and CM, 5 cats with asymptomatic CM and 15 healthy cats.
2020-07-19 | PXD017761 | Pride
Project description:A traditional Chinese medicine (TCM) formula, containing Astragalus membranaceus (Fisch.) Bunge, Aconitum wilsonii Stapf ex Veitch, Curcuma longa L., and Radix ophiopogonis (AACO), has clinically proven therapeutic value for the treatment of chronic heart failure (CHF). In this study, we explored the potential pharmacological mechanism underlying the activity of the AACO formula against CHF.
2024-11-20 | GSE217747 | GEO
Project description:Particulate Matter Triggers Carotid Body Dysfunction, Respiratory Dysynchrony and Cardiac Arrhythmias in Mice with Cardiac Failure The mechanistic link between human exposure to airborne particulate matter (PM) pollution and the increased cardiovascular morbidity and mortality observed in people with congestive heart failure (CHF) is unknown. We now show that exposure of genetically-engineered mice with CHF (expressing a cardiac-specific CREB mutant transcription factor) to ambient PM (collected in Baltimore, mean aerodynamic diameter 1.9 um) unmasks severe autonomic morbidities manifested as significant reductions in heart rate variability, respiratory dysynchrony and increased frequency of serious ventricular arrhythmias, features not observed in PM-challenged wild type mice without CHF. PM exposure in CREB mice with CHF reflexly triggers autonomic dysfunction via heightened carotid body function as evidenced by pronounced afferent nerve responses to hypoxia and marked depression of breathing by hyperoxia challenge. Genomic analyses of lung and ventricular tissues revealed PM-induced molecular signatures of inflammation and oxidative stress. These findings in a murine model of cardiac failure provide the first direct assessment of autonomic function in response to PM challenge and are highly consistent with current epidemiologic findings on cardiovascular morbidity in susceptible PM-exposed human populations. We utilized a murine model of dilated cardiomyopathy to address potential mechanistic links between PM exposure and the development of life-threatening cardiac dysrhythmias.
2009-08-10 | GSE17478 | GEO
Project description:Background HIV is associated with elevated risk of heart failure ( HF ). Despite poor agreement between automated, administrative code-based HF definitions and physician-adjudicated HF , no studies have evaluated incident adjudicated HF for people living with HIV ( PLWH ). Methods and Results We analyzed PLWH and uninfected controls receiving care in an urban medical system from January 1, 2000, to July 12, 2016. Physicians reviewed data from medical records to adjudicate HF diagnoses. We used multivariable-adjusted Cox models to analyze incident HF for PLWH versus controls and HIV -related factors associated with incident HF . We also analyzed the performance of automated versus physician-adjudicated HF definitions. Incident adjudicated HF occurred in 97 of 4640 PLWH (2.1%; mean: 6.8 years to HF ) and 55 of 4250 controls (1.3%; mean: 6.7 years to HF ; multivariable-adjusted hazard ratio: 2.10; 95% confidence interval, 1.38-3.21). Among PLWH , higher HIV viral load ( hazard ratio per log10 higher time-updated viral load: 1.22; 95% confidence interval, 1.11-1.33) was associated with greater HF risk and higher CD 4+ T cell count was associated with lower HF risk ( hazard ratio per 100 cells/mm3 higher time-updated CD 4 count: 0.80; 95% confidence interval, 0.69-0.92). In exploratory analyses, the most accurate automated HF definitions had sensitivities of 67% to 75% and positive predictive values of 54% to 60%. Conclusions In a cohort with rigorous HF adjudication, PLWH had greater risks of HF than uninfected people after adjustment for demographics and cardiovascular risk factors. Higher HIV viral load and lower CD 4+ T cell count were associated with higher HF risk among PLWH . Automated methods of HF ascertainment exhibited poor accuracy for PLWH and uninfected people.
| S-EPMC6404176 | biostudies-literature
Project description:After induction of ischemic chronic heart failure (CHF), mice exhibited depression-like behavior, in terms of increased anhedonia, and decreased both exploratory activity and interest in novelty. On histology, ischemic CHF mice showed no alterations in overall cerebral morphology. To further evaluate relevant behavioral changes found in CHF mice, RNA-sequencing analysis of prefrontal cortex and hippocampus - the brain regions, whose structural and functional alterations are associated with an increased risk for developing major depressive disorder - and of left myocardial tissue was performed in CHF vs. sham-operated animals. RNA-sequencing revealed relevant changes in hippocampal or prefrontal cortical expression of genes responsible for axonal vesicle transport (Kif5b), signal transduction (Arc, Gabrb2), limitation of inflammation (RORA; Nr4a1) and of hypoxic brain damage (Hif3a). Besides, the actual literature describes some of the genes (RORA, Gabrb2, Npas4, and Junb) being associated with depression-like behavior. Nr4a1 significantly regulated in both brain and heart tissue after induction of ischemic CHF could be a potential link and reveals the central role of inflammation in the interrelation of the brain and the failing heart.
2015-02-20 | GSE55280 | GEO