Human PBMCs: Healthy vs Diabetic nephropathy vs ESRD
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PROVIDER: PRJNA595989 | ENA |
REPOSITORIES: ENA
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Project description:Transcriptional profiling of human PBMCs comparing healthy controls, patients with diabetic nephropathy and patients with ESRD. PBMCs were analyzed as they mediate inflammatory injury. Goal was to determine effects of increasing severity of diabetic nephropathy on global PBMC gene expression. Microarray analysis of PBMCs taken from patients with varying degrees of diabetic nephropathy.
2020-12-01 | GSE142153 | GEO
Project description:Background: Long-term complications of type 2 diabetes (T2D) are the major causes for T2D-related disability and mortality. Notably, diabetic nephropathy (DN) has become the most frequent cause of end-stage renal disease (ESRD) in most countries. Understanding epigenetic contributors to DN can provide novel insights into this complex disorder and lay the foundation for more effective monitoring tools and preventive interventions, critical for achieving the ultimate goal of improving patient care and reducing healthcare burden.
2022-03-31 | GSE186021 | GEO
Project description:Gene expression profiling in glomeruli from human kidneys with diabetic nephropathy Keywords = Diabetes Keywords = kidney Keywords = glomeruli Keywords: other
2004-04-01 | GSE1009 | GEO
Project description:diabetes, mouse models, diabetic nephropathy, streptozotocin db/db Keywords: other
2004-01-20 | GSE710 | GEO
Project description:Diabetic nephropathy and diabetic retinopathy are related. We used scRNA-seq and RNA-seq to analyze the cellular linkage between them.
2023-08-15 | GSE204880 | GEO
Project description:gut microbiome in diabetic nephropathy
| PRJEB36826 | ENA
Project description:In order to more accurately and objectively clarify the biological role of lncRNAs in diabetic nephropathy, we detected their expression profiles in renal tissues from patients with diabetic nephropathy.
2022-11-24 | GSE218344 | GEO
Project description:Diabetic nephropathy (DN) is a leading cause of ESRD worldwide, but its molecular pathogenesis is not well-defined and there are no specific treatments. In humans, there is a strong genetic component determining susceptibility to DN. However, specific genes controlling DN susceptibility in humans have not been identified. Here we describe a new mouse model, combining type 1 diabetes with activation of the renin angiotensin system (RAS), which develops robust kidney disease with features resembling human DN: heavy albuminuria, hypertension and glomerulosclerosis. Additionally, there is a powerful effect of genetic background regulating susceptibility to nephropathy. The 129 strain is susceptible to kidney disease, whereas the C57BL/6 strain is resistant. To examine the molecular basis of this differential susceptibility, we analyzed the glomerular transcriptome of young mice with albuminuria but without detectable alterations in glomerular structure. We find dramatic difference in regulation of immune and inflammatory pathways with up-regulation of pro-inflammatory pathways in the susceptible (129) strain and coordinate down-regulation in the resistant (C57BL/6) strain, compared to their respective baselines. Many of these pathways were also up-regulated in a rat model and in humans with DN. Our studies suggest that genes controlling inflammatory responses, triggered by hyperglycemia and hypertension, may be critical early determinants of susceptibility to DN. The analysis was carried out on 2 strains of mice (129/SvEv and C57BL/6), each involving 2 genotypes (wild-type and RenTg/Ins2Akita mutations). Four replicates were used for each strain-genotype (with the exception of 129/SvEv wild-type mice, which had 3 replicates).
2016-08-13 | E-GEOD-85569 | biostudies-arrayexpress
Project description:Background Dysfunction of the circadian clock has been implicated in the pathogenesis of a variety of diseases, including metabolic disorders, inflammatory conditions, and cancer. While the significance of circadian rhythm in diabetic nephropathy is gaining attention, the specific alterations in circadian profiles in diabetic nephropathy remain unexplored. Methods In the present study, we performed RNA sequencing on renal cortex samples collected every 4-hour across the day from both control and diabetic mice. The rhythmicity of genes was identified using the JTK_CYCLE algorithm for each group. Genes that lost, acquired, or sustained rhythmicity in diabetic mice were denoted the circadian dysregulation gene-set. Subsequent bioinformatic analyses focused on this gene set to investigate the circadian reprogramming in diabetic nephropathy. Results We observed significant circadian disruption in the kidney of diabetic mice, marked by both the gain and loss of rhythmicity, along with alterations in the phase and amplitude of genes that retained rhythmic expressions. Circadian disturbances such like phase shifts and alterations in relative amplitude or mesor, were noted in core clock genes. Furthermore, genes that lost rhythmicity in diabetic nephropathy were predominantly associated with protein homeostasis and glycolipid metabolism, whereas those that gained rhythmicity were mainly linked to gene regulation, fatty acid metabolism, and protein transport. The genes in the circadian dysregulation gene-set that exhibit differential expression at least at one Zeitgeber time, were most prominently enriched in lipid metabolic process. WGCNA and correlation analysis revealed co-expression networks involving core clock genes and PPAR signaling pathway with renal triglyceride levels. Conclusions Our study reveals substantial circadian disruption in diabetic nephropathy, with significant impacts on protein homeostasis and glycolipid metabolism. Furthermore, our findings highlight the potential influence of circadian system dysregulation on the disorder of fatty acid metabolism in diabetic nephropathy.
2026-02-18 | GSE283571 | GEO
Project description:We report the early transcriptional changes in human diabetic nephropathy by single nucleus RNA sequencing
2019-09-10 | GSE131882 | GEO