Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Molecular mechanisms of kidney injury in diabetic mice based on single-cell sequencing techniques

ABSTRACT: Molecular mechanisms of kidney injury in diabetic mice based on single-cell sequencing techniques

PROVIDER: PRJNA1101568 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28726265_1.fastq.gz	Fastqsanger.gz
	SRR28726265_2.fastq.gz	Fastqsanger.gz
	SRR28726266_1.fastq.gz	Fastqsanger.gz
	SRR28726266_2.fastq.gz	Fastqsanger.gz
	SRR28726267_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Molecular mechanisms of kidney injury in diabetic mice based on single-cell sequencing techniques

Project description:To investigate the pathogenic molecular mechanisms and signaling pathways of early diabetic kidney disease. We performed single-cell RNA sequencing on kidney tissue of early type 1 diabetic mice.

2024-07-31 | GSE264268 | GEO

Gene expression profile of mouse diabetic kidney disease (DKD) injury

Project description:Diabetic kidney disease (DKD) is a significant clinical challenge, with an increasing prevalence. Our research identified that fibroblast growth factor 4 (FGF4) secreted by podocytes is a key factor in a mouse model of DKD. Given the importance of FGF4 in DKD-induced kidney injury, we performed gene expression analysis on kidney tissues. This analysis compared db/db model mice with those treated with recombinant FGF4 (rFGF4). The results showed that, compared to the db/db model group, db/db mice treated with long-term rFGF4 demonstrated significant improvements in renal function markers, such as serum urea nitrogen and urinary protein levels.Overall, our findings indicate that FGF4 is a critical regulatory factor in DKD-induced renal injury, providing evidence that it alleviates glomerular damage by inhibiting oxidative stress and apoptosis.

2025-09-11 | GSE287026 | GEO

Gene expression profile of mouse diabetic kidney disease (DKD) injury

Project description:Gene expression profile of mouse diabetic kidney disease (DKD) injury

| PRJNA1211003 | ENA

Expression data from OVE26 diabetic mouse kidney

Project description:OVE26 mouse was chosen to study the progressive changes in renal gene expression because it displays the most advanced albuminuria mouse models that assembles advanced human diabetic nephropathy. OVE26 mice induce inflammatory gene expression changes consistent with advanced renal disease, associated with severe albuminuria and not reported in any other diabetic models. They provide the first opportunity in a model of diabetic nephropathy to assess the effect of induction of inflammatory proteins that have been implicated in renal injury. Microarray expression was performed on whole kidney from control and diabetic mice at 2, 4 and 8 months of age and validated by rtPCR, in situ hybridization or immunohistochemistry.

2010-04-06 | E-GEOD-20636 | biostudies-arrayexpress

Complement C5a/C5a receptor 1 induces renal injury in diabetic kidney disease via mitochondrial metabolic reprogramming

Project description:In mice, complement C5a and its receptor C5aR1 elicit systemic and local inflammation and drive tissue injury in diabetic kidney disease via altered metabolic flexibility, which can be attenuated by therapy with a specific orally active inhibitor of C5aR1.

2019-07-01 | GSE118089 | GEO

Roux-en-Y Gastric Bypass Reduces Podocyte Injury in Diabetic Kidney Disease

Project description:Podocyte injury in diabetic kidney disease contributes to the development of albuminuria and subsequent renal decline. Clinically, gastric bypass surgery is associated with reductions in albuminuria, and rodent studies demonstrate coherent improvements in renal histology. We aimed to investigate the mechanisms underpinning remission of albuminuria following gastric bypass focussing on podocyte injury. Firstly, we tracked the evolution of albuminuria and cognate evidence of histological and ultrastructural damage to the glomerulus in male Zucker Diabetic Fatty rats. Secondly, we examined the impact of gastric bypass in these rats, focussing on podocyte injury. Thirdly, we conducted a global transcriptomic study profiling the shift in the renal transcriptome in the Zucker Diabetic Fatty rats rat and its relevance to human disease. Lastly, we explored whether gastric bypass could reverse the changes seen in the disease associated transcriptome. Albuminuria in the Zucker Diabetic Fatty rat developed by 12 weeks of age. This was accompanied by glomerulomegaly, podocyte stress and ultrastructural evidence of podocyte dedifferentiation. When animals underwent gastric bypass at 12 weeks of age, marked reductions in albuminuria in association with normalisation of glomerular tuft size, attenuation of podocyte stress and improvements in podocyte foot process morphology were observed within 2 months of surgery. A characteristic disease associated gene expression signature was observed in the kidneys of Zucker Diabetic Fatty rats, with a core set of alterations conserved in global analysis of the human DKD transcriptome. Many of the shared gene expression alterations were reversed by gastric bypass. Reductions in podocyte injury represent a key mechanism underpinning the remission of albuminuria following gastric bypass.

2019-07-10 | GSE117085 | GEO

GPR124 Protects against Podocyte Senescence and Injury in Diabetic Kidney Disease

Project description:GPR124 Protects against Podocyte Senescence and Injury in Diabetic Kidney Disease

| PRJNA1180511 | ENA

Diabetic vs. Menopausal/diabetic kidney cortex

Project description:Gene expression in kidney cortex of diabetic mice and menopausal diabetic mice following 6 weeks of diabetes. Diabetes was induced with low-dose streptozotocin injections and menopause was induced by injection of 4-vinylcyclohexene diepoxide. Samples = 12

2010-09-14 | E-GEOD-20702 | biostudies-arrayexpress

Transcriptome Analysis of Human Diabetic Kidney Disease

Project description:This SuperSeries is composed of the following subset Series: GSE30528: Transcriptome Analysis of Human Diabetic Kidney Disease (DKD Glomeruli vs. Control Glomeruli) GSE30529: Transcriptome Analysis of Human Diabetic Kidney Disease (DKD Tubuli vs. Control Tubuli) GSE30566: Transcriptome Analysis of Human Diabetic Kidney Disease (Control Glomeruli vs. Control Tubuli) Refer to individual Series

2011-08-02 | E-GEOD-30122 | biostudies-arrayexpress

PAD4 promotes macrophage migration to aggravate tubulointerstitial injury in diabetic kidney disease [RNA-seq]

Project description:Peptidyl Arginine Deiminase 4 (PAD4) is an enzyme predominantly expressed in myeloid cells, and its role in diabetic kidney disease (DKD) remains unknown. We functionally characterized 48 PAD4 variants identified among 469,779 participants from UK Biobank and examined their associations with renal function. We found that 32 PAD4 variants causes loss of function, which was significantly associated with higher estimated glomerular filtration rate. We observed an enhanced PAD4 expression in renal tubulointerstitium among DKD patients and animal models of DKD. Both PAD4 deficiency in macrophages and PAD4 inhibitor GSK484 significantly alleviated renal tubulointerstitial injury by reducing macrophage infiltration in diabetic mice models. Mechanistically, PAD4 interacted with p65 to promote its binding to Cmklr1 promoter and induce the expression of Cmklr1, which led to an enhanced macrophage migration. These findings demonstrate the crucial role of PAD4-mediated macrophage migration in tubulointerstitial injury of DKD.

2025-10-16 | GSE279745 | GEO

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