Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Impact of chronic kidney disease (CKD) on heart remodeling after myocardial infarction (MI)

ABSTRACT: Uremic cardiomyopathy is a clinically highly relevant cause of cardiovascular events in patients with chronic kidney disease (CKD). Additionally, after acute myocardial infarction (MI), CKD-patients exhibit an increased risk of death. To investigate the underlying molecular mechanisms causing the adverse effects of CKD on cardicac outcome after MI, male mice were fed with an adenine-supplemented diet combined with western type diet (CKD mice) or with western type diet only (control mice). Invasive heart function evaluation and histological analyses were performed 7 days after MI-induction through left anterior descending artery (LAD) ligation. For a deeper look on molecular level, RNA sequencing of heart tissue was performed.

ORGANISM(S): Mus musculus

PROVIDER: GSE283464 | GEO | 2026/04/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Oxidative stress initiates hemodynamic change in CKD induced heart disease

Project description:Cardiovascular disease is highly prevalent in patients with chronic kidney disease (CKD) and responsible for approximately half of CKD-related deaths. The mechanisms underlying the detrimental impact of CKD on the heart are still incompletely understood, but CKD is associated with endocrinal, inflammatory and hemodynamic changes that impact the heart and may contribute to the development of uremic cardiomyopathy.

2025-01-17 | PXD050994 | Pride

Experimental mouse model of chronic kidney disease reveals altered cardiac oxidative stress responses in CKD

Project description:Uremic cardiomyopathy is a clinically highly relevant cause of cardiovascular events in patients with chronic kidney disease (CKD). This study aimed at a comprehensive analysis of cardiac function and cardiac pathological characteristics in adenine-induced CKD in 129/Sv mice. This included the analysis of kidney function and morphology, heart function as well as cardiac hypertrophy, fibrosis and calcification. Also, cardiac RNA-sequencing was performed. Although overall, no cardiac dysfunction, hypertrophy or fibrosis could be observed, prolonged moderate CKD in this mouse model enhanced cardiac oxidative stress markers. In line, cardiac RNA-sequencing revealed an increase in oxidative stress-inducing signaling in CKD as well as anti-inflammatory feedback responses. This suggests a maladaptive preconditioning of the heart in CKD, which could increase the risk of enhanced cardiovascular damage upon additional cardiovascular risk factors and/or events.

2022-09-21 | GSE191122 | GEO

Mitochondrial Proteomics in a murine model of CKD

Project description:This project involves TMT-labeled proteomics analysis of mitochondria isolated from skeletal muscle, heart, and kidney of mice with and without chronic kidney disease (CKD). CKD was induced by adenine-supplementation of the diet for 6 months. Mouse strain was C57BL6J mice from Jackson Lab, aged 6 months prior to start of the diet. Mitochondria were isolated from skeletal muscle, heart, and kidney and immediately snap frozen and stored at -80C until processing.

2021-10-06 | PXD021847 | JPOST Repository

Comparison of gene expression in cardiac macrophages from P1 or P14 mice 3 days following MI

Project description:Myocardial infarction (MI) leads to cardiomyocyte death, which triggers an immune response that clears debris and restores tissue integrity. In the adult heart, the immune system facilitates scar formation, which repairs the damaged myocardium but compromises cardiac function. In neonatal mice, the heart can regenerate fully without scarring following MI; however, this regenerative capacity is lost by P7. The signals that govern neonatal heart regeneration are unknown. By comparing the immune response to MI in mice at P1 and P14, we identified differences in the magnitude and kinetics of monocyte and macrophage responses to injury. Using a cell-depletion model, we determined that heart regeneration and neoangiogenesis following MI depends on neonatal macrophages. Neonates depleted of macrophages were unable to regenerate myocardia and formed fibrotic scars, resulting in reduced cardiac function and angiogenesis. Immunophenotyping and gene expression profiling of cardiac macrophages from regenerating and nonregenerating hearts indicated that regenerative macrophages have a unique polarization phenotype and secrete numerous soluble factors that may facilitate the formation of new myocardium. Our findings suggest that macrophages provide necessary signals to drive angiogenesis and regeneration of the neonatal mouse heart. Modulating inflammation may provide a key therapeutic strategy to support heart regeneration. Total RNA was isolated from CD11b+Ly6G- cells sorted from hearts 3 days following ligation of LAD. 6 samples total: Triplicates of cells from P1 mice and from P14 mice

2014-01-31 | E-GEOD-54530 | biostudies-arrayexpress

Impact of chronic kidney disease (CKD) on heart remodeling after myocardial infarction (MI)

Project description:Impact of chronic kidney disease (CKD) on heart remodeling after myocardial infarction (MI)

| PRJNA1194002 | ENA

Expression data from the heart of sham and CKD mice

Project description:High incidence of heart failure (HF) is a typical characteristic of chronic kidney disease (CKD). However, the pathogenesis of CKD-associated HF remains elusive. Here, we investigated the changes in myocardial energy metabolism in CKD mice and explored the underlying mechanisms. To examine genome wide transcriptional changes in the heart of CKD mice, we performed microarray analysis using the Affymetrix Clariom S mouse.

2019-03-16 | GSE126824 | GEO

Oxalobacter formigenes colonization slows the progression of CKD and reduces cardiac remodeling in CKD

Project description:Accumulation of oxalate in patients with chronic kidney disease (CKD) is associated with CKD progression and an increased risk of cardiac death. Whether reducing oxalate slows CKD progression and prevents cardiovascular complications remains unexplored. We colonized Oxalobacter formigenes (Oxf), an oxalate-degrading microbiome, in the intestines of control and CKD mice fed with 1% hydroxyproline for 23 weeks. RNA-seq analysis of heart tissues of CKD mice reveals dysregulated expression of metabolic pathways and Oxf colonization reverses these changes. These findings demonstrate that oxalate accumulation plays a role not only in CKD progression but also in cardiovascular complications.

2025-06-16 | GSE297087 | GEO

High phosphorus and low protein mediate medial artery calcification and calcific uremic arteriolopathy in CKD mice: Significance of p38 MAPK signaling

Project description:Medial artery calcification and calcific uremic arteriolopathy (CUA) are observed in patients with chronic kidney disease (CKD). They are strongly associated with increased morbidity and mortality, yet the underlying mechanisms are poorly understood, and no effective drug targets have been developed. Herein, we observed that a high phosphate, low protein (HPi-Lp) diet induced medial artery and skin arteriolar calcification in 5/6 nephrectomy (5/6 Nx) CKD mice. We further determined that p38 MAPK signaling was critical in this vasculopathy. Calcification was examined using a micro-CT scan, Alizarin Red staining, Von Kossa staining, and calcium assay. Additionally, we found that the HPi-Lp diet feeding aggravated glomerulus impairment and renal fibrosis in 5/6 Nx mice. Using RNA-Seq analysis, we identified that p38 MAPK signaling was specifically activated in the 5/6 Nx-HPi-Lp mice. Inactivation of p38 MAPK signaling using a pharmacological inhibitor SB203580 significantly reduced medial artery calcification, skin arteriolar calcium deposits, and kidney fibrosis. Collectively, our data suggest that 5/6 Nx mice fed a HPi-Lp diet can be used as a reliable mouse model for studying medial artery and CUA arteriolar calcification. Additionally, targeting p38 MAPK signaling could be a promising therapeutic strategy to mitigate these vascular disorders in patients with CKD.

2025-09-24 | GSE288848 | GEO

ATAC-seq Profiling of Adult Mouse Cardiomyocytes Treated with AAV9-cTnT-Rbm22 in MI Model

Project description:Purpose: The purpose of this study was to identify chromatin alterations regulated by RBM22 in adult mouse cardiomyocytes (AMCMs) after myocardial infarction (MI). We performed ATAC sequencing on AMCMs isolated from mice post-MI that were infected with either AAV9-cTnT-GFP (control viral vector, AAV9-Control) or AAV9-cTnT-Rbm22-GFP (AAV9-Rbm22). Methods: 8-week-old C57BL/6J mice underwent permanent ligation of the left anterior descending (LAD) coronary artery, followed immediately by intramyocardial injection of either AAV9-Control or AAV9-Rbm22 at the infarct border zone. Adult cardiomyocytes were isolated post-MI using the Langendorff perfusion method. Results: We identified differentially altered chromatin accessibility regions between adult cardiomyocytes injected with the indicated viral vectors post-MI.

2026-02-12 | GSE311241 | GEO

Evaluating the effects of cardiac telomerase re-activation after myocardial infarction in adult mice

Project description:Coronary heart disease is a main cause of death in the developed world and treatment success remains modest with high mortality rates within one year after myocardial infarction (MI). Thus, new therapeutic targets and effective treatments are necessary. Short telomeres are risk factors for age-associated diseases including heart disease. Here, we address the potential of telomerase (Tert) activation in prevention of heart failure after MI in adult mice. We use adeno-associated viruses for cardiac-specific Tert expression in a mouse model of MI. We find that upon MI, hearts expressing Tert show attenuated cardiac dilation, improved ventricular function and smaller infarct scars concomitant with increased mouse survival by 17% compared to controls. Furthermore, Tert treatment results in elongated telomeres, increased numbers of Ki67 and pH3-positive cardiomyocytes and a gene expression switch towards a regeneration signature of neonatal mice. Our work highlights telomerase activation as a novel therapeutic strategy to prevent heart failure after MI. Mice of one year of age were left untreated (control) or injected with 5*10^11 adeno associated viruses particles of serotype 9 (AAV9) that carry either en empty expression cassette or express telomerase under control of the CMV promoter. Virus injected mice then underwent myocardial infarction induced through permenant left anterior descending artery (LAD) ligation. Mice that survived for six weeks after LAD ligation were sacrificed and 4 hearts per group (AAV9-empty or AAV9-Tert) and 3 control hearts (no virus treatment, no ligation) were subjected to total RNA isolation for micro array analysis.

2014-12-15 | E-GEOD-62973 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data