Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR7253830.fastq.gz | Fastqsanger.gz | |||
| ERR7253840.fastq.gz | Fastqsanger.gz | |||
| ERR7253850.fastq.gz | Fastqsanger.gz | |||
| ERR7253860.fastq.gz | Fastqsanger.gz | |||
| ERR7253870.fastq.gz | Fastqsanger.gz |
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Project description:Patients with heart failure with preserved ejection fraction (HFpEF) often have an unfavorable cardiometabolic profile, and obesity-related HFpEF has become a well-recognized HFpEF sub-phenotype. Targeting this unfavorable cardiometabolic profile may therefore represent a rational treatment strategy. The glucagon-like peptide-1 receptor agonist (GLP1-RA) semaglutide has been shown to induce significant weight loss and to improve cardiovascular outcomes. In this study, we investigated the cardiometabolic effects of semaglutide in a representative mouse model of HFpEF and compared it to the effects of weight loss by caloric restriction.
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Project description:Identifying the regulatory mechanisms of genome-wide association study (GWAS) loci affecting adipose tissue has been restricted due to limited characterization of adipose transcriptional regulatory elements. We profiled chromatin accessibility in three frozen human subcutaneous adipose tissue needle biopsies and preadipocytes and adipocytes from the Simpson Golabi-Behmel Syndrome (SGBS) cell strain using an assay for transposase-accessible chromatin (ATAC-seq). We identified 68,571 representative accessible chromatin regions (peaks) across adipose tissue samples (FDR<5%). GWAS loci for eight cardiometabolic traits were enriched in these peaks (p<0.005), with the strongest enrichment for waist-hip ratio. Of 110 recently described cardiometabolic GWAS loci colocalized with adipose tissue eQTLs, 59 loci had one or more variants overlapping an adipose tissue peak. Annotated variants at the SNX10 waist-hip ratio locus and the ATP2A1-SH2B1 body mass index locus showed allelic differences in regulatory assays. These adipose tissue accessible chromatin regions elucidate genetic variants that may alter adipose tissue function to impact cardiometabolic traits.
2019-01-01 | GSE110734 | GEO
Project description:Obesity and diabetes are linked to cardiometabolic diseases, however study in this field faces hardships as there are substantial prognostic heterogeneity involved. To profile the molecular mechanisms that contribute to the different responses to bariatric surgery dependent on the presence of diabetes, we sought to identify extracellular vesicular proteomic signatures of obesity with or without diabetes before or after bariatric surgery. In this study, extracellular vesicle proteins in 30 morbidly obese patients with (n = 12) or without (n = 18) diabetes were sampled before or 6 months after bariatric surgery and were compared to those in 37 healthy controls, analyzed by using the SWATH-MS analysis.
2025-10-06 | PXD040143 | Pride
Project description:Aims: Heart failure with preserved ejection fraction (HFpEF) is a multifactorial disease that constitutes several distinct phenotypes, including a common cardiometabolic phenotype with obesity and type 2 diabetes mellitus. Treatment options for HFpEF are limited, and development of novel therapeutics is hindered by the paucity of suitable preclinical HFpEF models that recapitulate the complexity of human HFpEF. Metabolic drugs, like Glucagon Like Peptide Receptor Agonist (GLP-1RA) and Sodium Glucose Transporter 2 inhibitors (SGLT2i), have emerged as promising drugs to restore metabolic perturbations and may have value in the treatment of the cardiometabolic HFpEF phenotype. We aimed to develop a multifactorial HFpEF mouse model that closely resembles the cardiometabolic HFpEF phenotype, and evaluated the GLP-1 RA liraglutide and a SGLT2i dapagliflozin. Methods&Results: Aged (18-22 months old) female C57BL/6J mice were fed a standardized chow (CTRL) or high fat diet (HFD) for 12 weeks. After 8 weeks HFD, Angiotensin-II (ANGII), was administered for 4 weeks via osmotic mini-pumps. HFD+ANGII resulted in a cardiometabolic HFpEF phenotype, including obesity, impaired glucose handling and metabolic dysregulation with inflammation. The multiple-hit resulted in typical clinical HFpEF features, including cardiac hypertrophy and fibrosis with preserved fractional shortening but with impaired myocardial deformation, atrial enlargement lung congestion, and elevated blood pressures. Treatment with liraglutide attenuated the cardiometabolic dysregulation and improved cardiac function, with reduced cardiac hypertrophy, less myocardial fibrosis, and attenuation of atrial weight, natriuretic peptide levels, and lung congestion. Dapagliflozin treatment improved glucose handling, but had mild effects on the HFpEF phenotype. Conclusions: We developed a mouse model that recapitulates the human HFpEF disease, providing a novel opportunity to study disease pathogenesis and development of enhanced therapeutic approaches. We furthermore show that attenuation of cardiometabolic dysregulation may represent a novel therapeutic target for treatment of HFpEF.
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Project description:MetaCardis: EU-funded investigation into effects of gut microbiota in cardiometabolic diseases
http://www.metacardis.net/
2021-09-01 | MSV000088043 | MassIVE