Role of diet in cardiac aging and fibrosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA559176 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9920920.fastq.gz | Fastqsanger.gz | |||
| SRR9920921.fastq.gz | Fastqsanger.gz | |||
| SRR9920922.fastq.gz | Fastqsanger.gz | |||
| SRR9920913.fastq.gz | Fastqsanger.gz | |||
| SRR9920923.fastq.gz | Fastqsanger.gz |
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Project description:Calorie restriction (CR) improved healthspan in two longitudinal studies in nonhuman primates (NHPs), yet only the University of Wisconsin (UW) study demonstrated an increase in survival in CR monkeys relative to controls; the National Institute on Aging (NIA) study did not. Here, analysis of left ventricle samples showed that CR did not reduce cardiac fibrosis relative to controls. However, there was a 5.9-fold increase of total fibrosis in UW hearts, compared to NIA. Diet composition was a prominent difference between the studies; therefore, we used the NHP diets to characterize diet-associated molecular and functional changes in the hearts of mice. Consistent with the findings from the NHP samples, mice fed UW or a modified NIA diet with increased sucrose and fat developed greater cardiac fibrosis compared to the NIA diet, and transcriptomics analysis revealed diet-induced activation of myocardial oxidative phosphorylation and cardiac muscle contraction pathways.
2019-08-09 | GSE135532 | GEO
Project description:Role of cytokines in cardiac fibrosis and exercise
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Project description:The role of TMEM43 in cardiac fibrosis and dysfunction
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Project description:During acute sympathetic stress, the overeactivation of β-adrenergic receptors (β-ARs) caused cardiac fibrosis, by triggering inflammation and cytokine expression. It is unknown whether exercise training inhibited acute β-AR overactivation-induced cytokine expression and cardiac injury. Here, we reported that running exercise inhibited cardiac fibrosis and improved cardiac function in mice treated by isoproterenol, a β-AR agonist. Cytokine antibody array revealed that exercise prevented the expression changes of most cytokines induced by isoproterenol. Specifically, 18 ISO-upregulated and 3 ISO-downregulated cytokines belonged to six families (eg. chemokine) were prevented. A further KEGG analysis of these cytokines revealed that Hedgehog and Rap1 signaling pathways were involved in the regulation of cytokine expression by exercise. The expression changes of some cytokines that were prevented by exercise were verified by ELISA and real-time PCR. In conclusion, running exercise prevented the cytokine changes following acute β-AR overactivation and therefore attenuated cardiac fibrosis.
2019-03-30 | GSE129022 | GEO
Project description:Deletion of Tmem43 encoding nuclear membrane protein TMEM43, specifically in mouse cardiac myocytes leads to cardiac fibrosis and dysfunction. Temporal RNA-seq identified early and late trascriptomic changes and implicates TGFb1 in the pathogenesis of ACM caused by Tmem43 haploinsufficiency.
2021-02-26 | GSE147317 | GEO
Project description:We wanted to understand how a salt restriction diet could improve cardiac damage (ie cardiac hypertrophy, fibrosis, hypertension) in a rat model of metabolic syndrome. We thus performed an Agilent microarray experiment in order to identify expression variations in left ventricles of rats having a normal sodium diet (0,64%) or a low sodium diet (less than 0,01%)
2017-04-20 | GSE84524 | GEO
Project description:Fibrotic changes in the myocardium and cardiac arrhythmias represent fatal complications in rheumatic disease systemic sclerosis (SSc), however the underlying mechanisms remain elusive. Fos-related antigen-2 (Fosl-2) has been implicated in development of organ fibrosis. Mice overexpressing Fosl-2 (Fosl-2tg) showed interstitial cardiac fibrosis, disorganized connexin43/40 in intercalated discs and deregulated expression of genes controlling conduction system. Fosl-2tg mice developed higher heart rate (HR), prolonged QT intervals, arrhythmias with prevalence of premature ventricular contractions, ventricular tachycardias, II-degree atrio-ventricular blocks and reduced HR variability. Following stimulation with isoproterenol Fosl-2tg mice showed impaired HR response. To assess the role of inflammation in cardiac fibrosis we used Rag2-/-Fosl-2tg mice lacking T/B cells. These mice showed no myocardial fibrosis and ECG abnormalities. Transcriptomics analysis of cardiac Rag-2-/-Fosl-2wt/Rag2-/-Fosl-2tg/Fosl-2tg fibroblasts revealed that systemic inflammation triggered fibrotic and arrhythmogenic alterations while Fosl-2-overexpression mediated profibrotic signature. In human cardiac fibroblasts FOSL-2-overexpression enhanced myofibroblast signature under proinflammatory or profibrotic stimuli. These results demonstrate that under immunofibrotic conditions activator protein 1 transcription factor component Fosl-2 exaggerates myocardial fibrosis, arrhythmias and aberrant response to stress.
2022-10-27 | E-MTAB-12271 | biostudies-arrayexpress
Project description:Increasing age enhances the liver's vulnerability to nonalcoholic steatohepatitis (NASH) with fibrosis. Unraveling the intricate molecular relationship among aging, cellular senescence, and NASH is critical for developing effective treatments, yet it remains a daunting challenge. Here we report a vital epigenetic mechanism that links liver aging to NASH fibrosis. We find that up-regulation of a chromatin remodeler BAZ2B in a subpopulation of hepatocytes contributes to the pathological progression of NASH in patients. Genetic ablation or hepatocyte-specific knockdown of Baz2b rejuvenates hepatic cells and limits diet-induced steatohepatitis and liver fibrosis via preserving the peroxisome proliferator-activated receptor α (PPARα)-mediated lipid metabolism, which was impaired in both naturally aging and NASH mouse livers. Mechanistically, Baz2b down-regulates the expression of genes related to the PPARα signaling pathway by directly binding their promoter regions and reducing chromatin accessibility. Our study thus unravels the BAZ2B-PPARα-lipid-metabolism signal axis as a key pathway linking liver aging to NASH fibrosis, suggesting that BAZ2B is a potential therapeutic target for hepatic fibrosis.
2025-03-12 | GSE280663 | GEO
Project description:Translational control of cardiac fibrosis
| PRJNA542667 | ENA
Project description:1.1 Introduction Cardiac fibrosis occurs in a wide range of cardiac diseases and is characterised by the transdifferentiation of cardiac fibroblasts into myofibroblasts these cells produce large quantities of extracellular matrix, resulting in myocardial scar. The profibrotic process is multi-factorial, meaning identification of effective treatments has been limited. The antifibrotic effect of the bile acid ursodeoxycholic acid (UDCA) is established in cases of liver fibrosis however its mechanism and role in cardiac fibrosis is less well understood. 1.2 Methods In this study, we used cellular models of cardiac fibrosis and living myocardial slices to characterise the macroscopic and cellular responses of the myocardium to UDCA treatment. We complemented this approach by conducting RNA-seq on cardiac fibroblasts isolated from dilated cardiomyopathy patients. This allowed us to gain insights into the mechanism of action and explore whether the IL-11 and TGFβ/ WWP2 profibrotic networks are influenced by UDCA. Finally, we used fibroblasts from a TGR5 KO mouse to confirm the mechanism of action. 1.3 Results and Discussion We found that UDCA reduced myofibroblast markers in rat and human fibroblasts and in living myocardial slices, indicating its antifibrotic action. Furthermore, we demonstrated that the treatment of UDCA successfully reversed the profibrotic IL-11 and TGFβ/ WWP2 gene networks. We also show that TGR5 is the most highly expressed UDCA receptor in cardiac fibroblasts. Utilising cells isolated from a TGR5 knock-out mouse, we identified that the antifibrotic effect of UDCA is attenuated in the KO fibroblasts. This study combines cellular studies with RNA-seq and state-of-the-art living myocardial slices to offer new perspectives on cardiac fibrosis. Our data confirm that TGR5 agonists, such as UDCA, offer a unique pathway of action for the treatment of cardiac fibrosis. Medicines for cardiac fibrosis have been slow to clinic and have the potential to be used in the treatment of multiple cardiac diseases. UDCA is well tolerated in the treatment of other diseases, indicating it is an excellent candidate for further in-human trials.
2024-11-30 | E-MTAB-14602 | biostudies-arrayexpress