Dataset's files
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| GSE294519_Normalization_data_allsamples.txt.gz | Txt |
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Similar Datasets
Project description:To explore the role of SIRT6 in renal tubular epithelial cells in DKD mice, we extracted primary renal tubular epithelial cells from wild-type and tubular epithelial SIRT6-specific knockout DKD mice, respectively.
2026-07-08 | GSE291755 | GEO
Project description:To explore the role of SIRT6 in renal tubular epithelial cells in DKD mice, we extracted primary renal tubular epithelial cells from wild-type and tubular epithelial SIRT6-specific knockout DKD mice, respectively.
2026-07-08 | GSE291844 | GEO
Project description:Persistently enhancement of glycolytic activity has been increasingly implicated as a key contributor to the development of diabetic kidney disease (DKD). Lactate, the end product of glycolysis, can trigger histone lactylation, —an emerging epigenetic modification involved in regulating gene expression, yet its functional significance in DKD remains largely unclear. Here, we observed that 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), a key glycolytic enzyme, was remarkably induced in tubular epithelial cells (TECs) in both DKD patients and mice model. Inhibition the expression of PFKFB3 mitigated kidney fibrosis, and preserved kidney function in DKD mice model. Conversely, upregulation of PFKFB3 aggravates renal fibrogenesis and promotes the deterioration of renal pathology. Moreover, we demonstrated that reducing the lactate levels markedly alleviated renal fibrosis in DKD. Mechanistically, lactate generated via PFKFB3-driven glycolytic reprogramming selectively enhances H4K12 lactylation at the HIPK2 promoter, thereby activating its transcription and driving renal fibrotic progression. These findings suggest that tubular PFKFB3 enhancing HIPK2 expression by promoting H4K12la-mediated gene transcription. Thus, targeting the PFKFB3-mediated HIPK2 activation in renal tubular cells could be a novel strategy for DKD.
2026-04-22 | GSE328635 | GEO
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
Project description:We identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli; 330 probesets were commonly differentially expressed in both compartments. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in an additional set of DKD samples. Affymetrix expression arrays were used to identify differentially regulated transcripts in 44 microdissected human kidney samples. Stringent statistical analysis using the Benjamini_Hochberg corrected 2-tailed t-test was used to identify differentially expressed transcripts in control and diseased glomeruli and tubuli. This Series includes DKD and control glomeruli samples.
2011-08-02 | E-GEOD-30528 | biostudies-arrayexpress
Project description:We identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli; 330 probesets were commonly differentially expressed in both compartments. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in an additional set of DKD samples. Affymetrix expression arrays were used to identify differentially regulated transcripts in 44 microdissected human kidney samples. Stringent statistical analysis using the Benjamini_Hochberg corrected 2-tailed t-test was used to identify differentially expressed transcripts in control and diseased glomeruli and tubuli. This Series includes DKD and control tubuli samples.
2011-08-02 | E-GEOD-30529 | biostudies-arrayexpress
Project description:Diabetic kidney disease (DKD) is the leading cause of end-stage kidney disease (ESKD), and few treatment options are available today to prevent the progressive loss of renal function. Tubular abnormalities may precede glomerular pathology early and indicate the functional progression of DKD, however, pathological mechanisms that initiate tubular abnormalities are poorly understood. Here, we found that glucagon receptor (Gcgr) is specifically and highly expressed in proximal tubular cells (PTEC) of kidney. Glucagon injection exacerbated lipid accumulation, glycogen content, inflammation, fibrosis, and renal injury, along with morphology changes on proximal tubules, podocytes, glomerular basement membrane (GBM), and mitochondria in the early phase of DKD mice. Whereas, the specific knockdown or knockout of Gcgr in PTEC of kidney almost completely halted the development of DKD. In contrary to the effect of short-term glucagon stimulation on fatty acid oxidation, long-term glucagon exposure led to glucagon reversal in PTEC, which is characterized by reduced energy production and promoted lipogenesis, and this effect was through the Gcgr-PKA-Creb-mTOR pathway. Accordingly, anti-GCGR antibody treatment greatly blocked the pathogenesis of DKD induced by both type 2 and type 1 diabetes. Thus, our results revealed a novel role of glucagon/GCGR signaling in PTEC lipogenesis and DKD, and Gcgr would be a promising therapeutic drug target for the treatment of DKD.
2025-07-18 | GSE253774 | GEO
Project description:Diabetic kidney disease (DKD) has become the leading cause of end-stage renal disease worldwide. Therefore, efforts to understand DKD pathophysiology and prevent its development at the early phase are highly warranted. Here, we analyzed kidneys from healthy mice, diabetic mice, and diabetic mice treated with the sodium-glucose cotransporter 2 inhibitor dapagliflozin. Our combined method of ATAC and RNA sequencing revealed Csf2rb, Btla, and Isg15 as the key candidate genes associated with hyperglycemia, azotemia, and albuminuria. Their protein levels were altered together with multiple other inflammatory cytokines in the diabetic kidney, which was alleviated by dapagliflozin treatment. Cell culture of immortalized renal tubular cells and macrophages unraveled that dapagliflozin could directly effect on these cells in vitro as an anti-inflammatory agent independent of glucose concentrations. We further proved that dapagliflozin attenuated ischemia/reperfusion-induced chronic kidney injury and renal inflammation in mice. Overall, our data emphasize the importance of inflammatory factors to the pathogenesis of DKD, and provide valuable mechanistic insights into the renoprotective role of dapagliflozin.
2023-11-02 | GSE246576 | GEO
Project description:Diabetic kidney disease (DKD) has become the leading cause of end-stage renal disease worldwide. Therefore, efforts to understand DKD pathophysiology and prevent its development at the early phase are highly warranted. Here, we analyzed kidneys from healthy mice, diabetic mice, and diabetic mice treated with the sodium-glucose cotransporter 2 inhibitor dapagliflozin. Our combined method of ATAC and RNA sequencing revealed Csf2rb, Btla, and Isg15 as the key candidate genes associated with hyperglycemia, azotemia, and albuminuria. Their protein levels were altered together with multiple other inflammatory cytokines in the diabetic kidney, which was alleviated by dapagliflozin treatment. Cell culture of immortalized renal tubular cells and macrophages unraveled that dapagliflozin could directly effect on these cells in vitro as an anti-inflammatory agent independent of glucose concentrations. We further proved that dapagliflozin attenuated ischemia/reperfusion-induced chronic kidney injury and renal inflammation in mice. Overall, our data emphasize the importance of inflammatory factors to the pathogenesis of DKD, and provide valuable mechanistic insights into the renoprotective role of dapagliflozin.
2023-11-02 | GSE246763 | GEO
Project description:Acute kidney injury (AKI) have been thought to be reversible condition, however, emerging evidence demonstrated association between AKI and subsequent development of irreversible fibrosis and chronic kidney disease. In the present study, since recovery of AKI depends on renal tubular regeneration, factors expressing in renal tubules in adaptive or maladaptive repair process were investigated to predict reversibility of kidney injury. In the kidney of female F344 rats subjected to ischemia/reperfusion (I/R), regenerative tubules and dilated tubules were observed at 3 and 7 days after I/R. In fibrotic areas of the kidney of male SD rats subjected to I/R, renal tubules were dilated or atrophied. From microarray data of regenerative tubules, survivin, sex-determining region Y (SRY)-box 9 (SOX9), and CD44 were extracted as factors possibly relating to tubular regeneration or fibrosis. Immunohistochmical analysis demonstrated that survivin and SOX9 expressed in regenerative tubules, while SOX9 also expressed in renal tubules in fibrotic area, indicating that survivin and SOX9 contribute renal tubular regeneration, but sustained SOX9 expression may lead fibrosis. CD44 expressed in dilated tubules at day 3 and 7, and tubules in fibrotic area, suggesting that CD44 expressed in maladaptive tubules. These information will be helpful to consider reversibility of kidney injury.
2020-06-01 | GSE148420 | GEO