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Cardiac Transcriptomic Changes Induced by Early CKD in Mice Reveal Novel Pathways Involved in the Pathogenesis of Cardiorenal Syndrome Type 4

ABSTRACT: Cardiac Transcriptomic Changes Induced by Early CKD in Mice Reveal Novel Pathways Involved in the Pathogenesis of Cardiorenal Syndrome Type 4

PROVIDER: PRJNA987561 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25023200_1.fastq.gz	Fastqsanger.gz
	SRR25023200_2.fastq.gz	Fastqsanger.gz
	SRR25023201_1.fastq.gz	Fastqsanger.gz
	SRR25023201_2.fastq.gz	Fastqsanger.gz
	SRR25023202_1.fastq.gz	Fastqsanger.gz

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Cardiac Transcriptomic Changes Induced by Early CKD in Mice Reveal Novel Pathways Involved in the Pathogenesis of Cardiorenal Syndrome Type 4

Project description:Cardiorenal syndrome (CRS) type 4 is prevalent among the chronic kidney disease (CKD) population, with many patients dying from cardiovascular complications. However, limited data regarding cardiac transcriptional changes induced early by CKD is available. We used a murine unilateral ureteral obstruction (UUO) model to evaluate cardiac transcriptional regulation at 21 days post-surgery through RNA-seq and bioinformatics. UUO leads to significant kidney injury, low uremia, and pathological cardiac remodeling. RNA-seq analysis identified 76 differentially expressed genes (DEGs) in UUO hearts. Upregulated DEGs were significantly enriched in cell cycle and cell division pathways, immune responses, cardiac repair, inflammation, proliferation, oxidative stress, and apoptosis. Gene Set Enrichment Analysis further revealed mitochondrial oxidative bioenergetic pathways, autophagy, and peroxisomal pathways are downregulated in UUO hearts. Vimentin was also identified as an UUO-upregulated transcript. Our results emphasize the relevance of extensive transcriptional and epigenetic changes, mitochondrial dysfunction, homeostasis deregulation, fatty-acid metabolism alterations, and vimentin upregulation in CRS type 4 development.

2024-03-22 | GSE235751 | GEO

Cardiac transcriptomic changes induced by early CKD in mice reveal novel pathways involved in the pathogenesis of Cardiorenal syndrome type 4.

Project description:BackgroundCardiorenal syndrome (CRS) type 4 is prevalent among the chronic kidney disease (CKD) population, with many patients dying from cardiovascular complications. However, limited data regarding cardiac transcriptional changes induced early by CKD is available.MethodsWe used a murine unilateral ureteral obstruction (UUO) model to evaluate renal damage, cardiac remodeling, and transcriptional regulation at 21 days post-surgery through histological analysis, RT-qPCR, RNA-seq, and bioinformatics.ResultsUUO leads to significant kidney injury, low uremia, and pathological cardiac remodeling, evidenced by increased collagen deposition and smooth muscle alpha-actin 2 expression. RNA-seq analysis identified 76 differentially expressed genes (DEGs) in UUO hearts. Upregulated DEGs were significantly enriched in cell cycle and cell division pathways, immune responses, cardiac repair, inflammation, proliferation, oxidative stress, and apoptosis. Gene Set Enrichment Analysis further revealed mitochondrial oxidative bioenergetic pathways, autophagy, and peroxisomal pathways are downregulated in UUO hearts. Vimentin was also identified as an UUO-upregulated transcript.ConclusionsOur results emphasize the relevance of extensive transcriptional changes, mitochondrial dysfunction, homeostasis deregulation, fatty-acid metabolism alterations, and vimentin upregulation in CRS type 4 development.

| S-EPMC10950824 | biostudies-literature

CKD Rats

Project description:CKD Rats

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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

CKD Rats

Project description:Comparative gene expression profiling analysis of RNA-seq data for NC rats, adenine-induced CKD rats, and drug-treated CKD rats.

2024-03-14 | GSE261354 | GEO

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

Molecular Mediators of Cardiac Pathology in Cardiorenal Syndrome Type 4

Project description:Molecular Mediators of Cardiac Pathology in Cardiorenal Syndrome Type 4

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Quantitative proteomic analysis of CKD urine samples

Project description:Urinary proteomics studies have primarily focused on identifying markers of chronic kidney disease (CKD) progression. Here, we aimed to specify CKD-related injury markers through proteomics analysis in urine of patients with CKD. Label-free quantitative proteomics analysis based on liquid chromatography-tandem mass spectrometry was performed on urine samples obtained from 6, 9, 11, and 10 patients in health control, CKD stage 1, 3 and 5, respectively.

2021-01-19 | PXD016433 | Pride

microRNA in chronic kidney disease (CKD)

Project description:microRNA in chronic kidney disease (CKD)

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Glomerular filtrate proteins in acute cardiorenal syndrome

Project description:Acute cardiorenal syndrome (CRS-1) is a morbid complication of acute cardiovascular disease. Mechanistic investigations have focused on intrarenal cellular signaling induced by ischemia/reperfusion. Additional cardiorenal connector signals have been postulated, but investigation in CRS-1 has been limited by a paucity of animal models and technical limitations precluding discovery studies of glomerular filtrate. To address these limitations, we developed a translational model of CRS-1, cardiac arrest and cardiopulmonary resuscitation (CA/CPR) in mice. Quantitative proteomics using isobaric tagging (10-plex TMT reagents, Thermo Fisher) was performed on 24h urine collections from mice with deficient tubular endocytosis and from littermate controls, before and after CA/CPR. Data acquisition used the SPS MS3 method on a Thermo Fusion Tribrid mass spectrometer for accurate reporter ion signals. The findings confirmed CA/CPR-specific cardiac proteins in urine and identified a novel CA/CPR-specific filtrate component: Cardiac LIM protein (CSRP3).

2019-02-27 | PXD012193 | Pride

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