Single-cell RNA transcriptomics of hypertensive nephropathy patients
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA868215 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21002189_1.fastq.gz | Fastqsanger.gz | |||
| SRR21002189_2.fastq.gz | Fastqsanger.gz | |||
| SRR21002190_1.fastq.gz | Fastqsanger.gz | |||
| SRR21002190_2.fastq.gz | Fastqsanger.gz | |||
| SRR21002191_1.fastq.gz | Fastqsanger.gz |
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Project description:Hypertensive nephropathy (HTN) emerges as one of the leading causes of end-stage renal disease, yet the precise mechanisms and cell-specific gene expression changes are still unknown. This study used single-cell RNA sequencing (scRNA-seq) to explore novel molecular mechanisms and hub gene targets for HTN.Our data identifies a distinct cell-specific gene expression profile, pathogenic signaling pathways and potential cell-cell crosstalks in the progression of HTN. These findings will provide a promising novel landscape for mechanisms and treatment of HTN.
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Project description:Hypertensive nephropathy (HTN) is one of the leading causes of end-stage renal disease, yet the precise mechanisms and cell-specific gene expression changes are still unknown. This study used single-cell RNA sequencing (scRNA-seq) to explore novel molecular mechanisms and gene targets for HTN.Our data identifies a distinct cell-specific gene expression profile, pathogenic signaling pathways and potential cell-cell communications in the pathogenesis of HTN. These findings will provide a promising novel landscape for mechanisms and treatment of HTN.
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Project description:Hypertensive nephropathy is a common complication of hypertension that places a heavy burden on society. SGLT2 inhibitors are a new class of hypoglycemic agents that have been shown to have specific protective effects on the kidneys. This study aimed to investigate the early changes in renal transcription spectrum in spontaneously hypertensive rats and the effects of DAPA, a sodium-glucose cotransporter 2 inhibitor, on the remission of hypertensive nephropathy and its underlying molecular mechanisms. We furthermore show thatSGLT2 inhibitors may reduce inflammation and improve energy metabolism by regulating the expression of SLC9a3, Zbtb20, Trim50 and Ccnl2.
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Project description:Hypertensive nephropathy (HN) is a leading cause of chronic kidney disease (CKD), but molecular mechanisms underlying disease progression remain poorly understood. We aimed to identify transcriptomic signatures associated with disease progression and to localize these signatures within renal architectures. Patients with biopsy-proven HN were selected from the Norwegian Kidney Biopsy Registry and stratified after ≥5 years of follow-up into early stable (ES), early progressor (EP), late stable (LS) and late progressor (LP) based on baseline kidney function and annual eGFR decline. Bulk transcriptomic profiling was performed in a discovery cohort and validated in an independent cohort using nCounter profiling. Spatial transcriptomics was applied to map progression-associated signatures to nephron compartments. Bulk RNA sequencing identified 415 differentially expressed genes (DEGs) between ES and EP, and 692 between LS and LP samples. ES was enriched in circadian rhythm pathways, with reduced NR1D1 and NR1D2 expression in EP. LP was associated with metabolic reprogramming including glutathione, retinol and amino acid metabolism. Random forest modelling identified NR1D1 gene expression as a key classifier, validated in an independent cohort. Spatial transcriptomics revealed nephron segment-specific expression patterns, including a proximal tubule cluster enriched in ferroptosis in LP. Comparative nephron-segment analyses across groups revealed progression-associated biomarkers, including CHGA, CCN2 and SFRP2 in glomeruli, and APOE in proximal tubules. HN progression appears to involve stage-specific and compartmentalized molecular programs. Integration of bulk and spatial transcriptomics identifies candidate biomarkers and pathways, potentially supporting innovative prognostic stratification and therapeutic strategies.
2026-07-22 | GSE339455 | GEO
Project description:Background: Coenzyme Q10 (COQ10) nephropathy is a well-known cause of hereditary steroid-resistant nephrotic syndrome (SRNS), primarily impacting podocytes. This study aimed to elucidate variations in individual cell-level gene expression in COQ10 nephropathy using single-cell transcriptomics. Methods: We conducted single-cell sequencing of kidney biopsy specimen on a 5-year-old boy diagnosed with a COQ10 nephropathy caused by compound heterozygous COQ2 mutation. The analysis focused on the proportion of cell types, differentially expressed genes in each cell type, changes in gene expression related to mitochondrial function and oxidative phosphorylation (OXPHOS), and pathway analysis. Results: Our findings revealed a uniform downregulation of mitochondrial gene expression across various cell types in the context of these mutations. Notably, there was a specific increase in glycolysis-related gene expression in podocytes. The study also highlighted an altered immune cell population proportion attributed to the COQ2 gene mutation. Pathway analysis indicated a downregulation in OXPHOS and an upregulation of various synthesis pathways, particularly in podocytes. Conclusion: This study enhances our understanding of the pathogenesis of COQ10 nephropathy and underscore potential therapeutic targets for primary COQ10 nephropathy.
2025-04-02 | GSE270701 | GEO
Project description:Hypertensive nephropathy (HN) is a leading cause of chronic kidney disease (CKD), but molecular mechanisms underlying disease progression remain poorly understood. We aimed to identify transcriptomic signatures associated with disease progression and to localize these signatures within renal architectures. Patients with biopsy-proven HN were selected from the Norwegian Kidney Biopsy Registry and stratified after ≥5 years of follow-up into early stable (ES), early progressor (EP), late stable (LS) and late progressor (LP) based on baseline kidney function and annual eGFR decline. Bulk transcriptomic profiling was performed in a discovery cohort and validated in an independent cohort using nCounter profiling. Spatial transcriptomics was applied to map progression-associated signatures to nephron compartments. Bulk RNA sequencing identified 415 differentially expressed genes (DEGs) between ES and EP, and 692 between LS and LP samples. ES was enriched in circadian rhythm pathways, with reduced NR1D1 and NR1D2 expression in EP. LP was associated with metabolic reprogramming including glutathione, retinol and amino acid metabolism. Random forest modelling identified NR1D1 gene expression as a key classifier, validated in an independent cohort. Spatial transcriptomics revealed nephron segment-specific expression patterns, including a proximal tubule cluster enriched in ferroptosis in LP. Comparative nephron-segment analyses across groups revealed progression-associated biomarkers, including CHGA, CCN2 and SFRP2 in glomeruli, and APOE in proximal tubules. HN progression appears to involve stage-specific and compartmentalized molecular programs. Integration of bulk and spatial transcriptomics identifies candidate biomarkers and pathways, potentially supporting innovative prognostic stratification and therapeutic strategies.
2026-07-22 | GSE339454 | GEO
Project description:Hypertensive nephropathy (HN) is a leading cause of chronic kidney disease (CKD), but molecular mechanisms underlying disease progression remain poorly understood. We aimed to identify transcriptomic signatures associated with disease progression and to localize these signatures within renal architectures. Patients with biopsy-proven HN were selected from the Norwegian Kidney Biopsy Registry and stratified after ≥5 years of follow-up into early stable (ES), early progressor (EP), late stable (LS) and late progressor (LP) based on baseline kidney function and annual eGFR decline. Bulk transcriptomic profiling was performed in a discovery cohort and validated in an independent cohort using nCounter profiling. Spatial transcriptomics was applied to map progression-associated signatures to nephron compartments. Bulk RNA sequencing identified 415 differentially expressed genes (DEGs) between ES and EP, and 692 between LS and LP samples. ES was enriched in circadian rhythm pathways, with reduced NR1D1 and NR1D2 expression in EP. LP was associated with metabolic reprogramming including glutathione, retinol and amino acid metabolism. Random forest modelling identified NR1D1 gene expression as a key classifier, validated in an independent cohort. Spatial transcriptomics revealed nephron segment-specific expression patterns, including a proximal tubule cluster enriched in ferroptosis in LP. Comparative nephron-segment analyses across groups revealed progression-associated biomarkers, including CHGA, CCN2 and SFRP2 in glomeruli, and APOE in proximal tubules. HN progression appears to involve stage-specific and compartmentalized molecular programs. Integration of bulk and spatial transcriptomics identifies candidate biomarkers and pathways, potentially supporting innovative prognostic stratification and therapeutic strategies.
2026-07-22 | GSE339456 | GEO
Project description:RATIONALE: Hypertension can lead to podocyte damage and subsequent apoptosis, eventually resulting in glomerulosclerosis. Although alleviating podocyte apoptosis has clinical significance for the treatment of hypertensive nephropathy, an effective therapeutic target has not yet been identified. The function of Septin4, a pro-apoptotic protein and an important marker of organ damage, is regulated by post-translational modification (PTM). However, the exact role of Septin4 in regulating podocyte apoptosis and its connection to hypertensive renal damage remains unclear. OBJECTIVE: We investigated the function and underlying mechanism of Septin4 in AngII-induced hypertensive nephropathy to discover a theoretical basis for targeted treatment. METHODS AND RESULTS: Using transgenic Septin4-K174Q mutant mice treated with the antioxidant Tempol, we found that hyperacetylation of the K174 site of Septin4 exacerbates AngII induced hypertensive renal injury resulting from oxidative stress. Proteomics and western blotting assays indicated that Septin4-K174Q activates the cleaved-PARP1-cleaved-Caspase3 pathway. In Septin4-knockdown human renal podocytes, Septin4-K174R, which mimics deacetylation at K174, rescues podocyte apoptosis induced by AngII. We conclude that Septin4, when activated through acetylation of K174 (K174Q), promotes hypertensive renal injury. Immunoprecipitation and mass spectrometry analyses identified SIRT2 as a deacetylase that interacts with the Septin4 GTPase domain and deacetylates Septin4-K174. In Sirt2-deficient mice and SIRT2-knockdown renal podocytes, Septin4-K174 remains hyperacetylated and exacerbates hypertensive renal injury. By contrast, in Rosa26-Sirt2-Flag (SIRT2-TG) mice and SIRT2-knockdown renal podocytes re-expressing wild-type SIRT2, Septin4-K174 is hypoacetylated and mitigates hypertensive renal injury. CONCLUSION: Septin4-K174R, which mimics deacetylation by SIRT2, inhibits the cleaved-PARP1-cleaved-Caspase3 pathway. Septin4-K174R acts as a renal protective factor, mitigating AngII-induced hypertensive renal injury. These findings indicate that Septin4-K174 is a potential therapeutic target for the treatment of hypertensive renal injury.
2022-12-05 | PXD038538 |