Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31980500_1.fastq.gz | Fastqsanger.gz | |||
| SRR31980500_2.fastq.gz | Fastqsanger.gz | |||
| SRR31980501_1.fastq.gz | Fastqsanger.gz | |||
| SRR31980501_2.fastq.gz | Fastqsanger.gz | |||
| SRR31980502_1.fastq.gz | Fastqsanger.gz |
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Project description:Background: Horses are one of the few animals that spontaneously develop atrial fibrillation (AF), making them a powerful model for studying AF mechanisms and treatment effects. Despite the initial effectiveness of treatment in both horses and humans, AF-induced atrial remodelling compromises long-term success. Observational studies have suggested that metformin reduces the risk of AF, but its effects on progressive AF-induced atrial remodelling have not yet been evaluated in a high-fidelity large animal model. Methods: Here, we employed a longitudinal horse model of tachypacing-induced self-sustained AF to characterize the electrical, molecular, and metabolic atrial changes over four months of disease, with and without metformin treatment. Electrophysiological and multi-omic approaches were combined with histology, echocardiography, biochemical and mitochondrial analyses to evaluate disease progression and treatment response. Results: The horse model replicated critical aspects of AF-induced atrial remodelling observed in humans, including electrical and structural changes. Despite upregulation of metabolic genes and proteins in AF, no significant ultrastructural mitochondrial changes were detected. Metformin-treated horses were less susceptible to AF and sustained a less complex AF substrate in the right atrium after four months of disease. These effects were associated with increased activity of the metabolic regulator, AMP-activated kinase (AMPK) , changes in metabolic pathways and modulation of ion-channel gene expression. Metformin did not appear to alter left atrial substrate remodelling. Conclusion: Metformin treatment conferred electrical protection in both the early and later stages of AF in a translationally relevant preclinical model. These findings support metformin as a lead molecul ar for AF-prevention, warranting further mechanistic and clinical studies.
2025-12-03 | PXD059963 | Pride
Project description:performing high-throughput RNA sequencing (RNA-Seq) transcriptomic analysis of hepatic cells after metformin or CWE treatment to identify changes in diabetes-related gene expression. Outcomes of this project provide evidence for the effectiveness of Ceylon cinnamon water extract compared to the current standard therapy for type 2 diabetes, metformin.
2022-02-14 | E-MTAB-11418 | biostudies-arrayexpress
Project description:The aim of the project was to identify the tissue-specific patterns of gene expression of selected horse tissues, derived from two germ layers, endodermal (liver and lung) and mesenchymal (cardiac striated muscle) origin.
2023-08-31 | GSE193661 | GEO
Project description:The aim of the project was to identify the tissue-specific DNA methylation patterns of selected horse tissues, derived from two germ layers, endodermal (liver and lung) and mesenchymal (cardiac striated muscle) origin. The comparative analysis of DNA methylation patterns of the genome fraction rich in CpG dinucleotides was investigated using Reduced Representation Bisulfite Sequencing (RRBS) technique.
2022-12-31 | GSE191047 | GEO
Project description:Metformin has been commonly used for decades to treat type 2 diabetes. Recent data indicates that mice treated with metformin live longer and healthier lives. Here, we show that chronic metformin exposure in mice and diabetics taking metformin have higher levels of the microRNA processing protein, Dicer. Examination of how metformin affects Dicer expression revealed that metformin alters binding of the AUF1 RNA-binding protein to DICER1 mRNA, which leads to stabilization of DICER1 mRNA. We found differential changes in microRNA expression in mice treated with metformin or caloric restriction, a proven life extending intervention. Several of these microRNAs are important for regulating cellular senescence and lifespan in model organisms. Consistent with this observation, treatment with metformin decreased cellular senescence in a Dicer-dependent manner. These data lead us to hypothesize that changes in Dicer levels may be important for organismal aging and that interventions that upregulate Dicer expression (e.g., metformin) may offer new therapeutic approaches to combat or prevent age-related diseases. Key words: diabetes mellitus, metformin, senescence, miRNA, RNA-binding proteins
2017-02-14 | GSE73393 | GEO
Project description:Metformin is the front-line treatment for type 2 diabetes worldwide. It acts via effects on glucose and lipid metabolism in metabolic tissues, leading to enhanced insulin sensitivity. Despite significant effort, the molecular basis for metformin response remains poorly understood, with a limited number of specific biochemical pathways studied to date. To broaden our understanding of hepatic metformin response, we combine phospho-protein enrichment in tissue from genetically engineered mice with a quantitative proteomics platform to enable the discovery and quantification of basophilic kinase substrates in-vivo. We define proteins that binding to 14-3-3 are acutely regulated by metformin treatment and/or loss of the serine/threonine kinase, LKB1. Inducible binding of 250 proteins following metformin treatment is observed, 44% LKB1-dependent. Beyond AMPK, metformin activates Protein Kinase D and MAPKAPK2 in an LKB1-independent manner, revealing additional kinases that may mediate aspects of metformin response. Deeper analysis uncovered substrates of AMPK in endocytosis and calcium homeostasis.
2019-10-07 | MSV000084429 | MassIVE