Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Kidney Single-Cell Atlas Reveals Macrophage Heterogeneity in Progression and Regression of Cisplatin Induced AKI [scRNA-seq]

ABSTRACT: Kidney Single-Cell Atlas Reveals Macrophage Heterogeneity in Progression and Regression of Cisplatin Induced AKI [scRNA-seq]

PROVIDER: PRJNA910961 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Kidney Single-Cell Atlas Reveals Macrophage Heterogeneity in Progression and Regression of Cisplatin Induced AKI.

Project description:Kidney Single-Cell Atlas Reveals Macrophage Heterogeneity in Progression and Regression of Cisplatin Induced AKI.

| PRJNA911169 | ENA

Kidney Single-Cell Atlas Reveals Macrophage Heterogeneity in Progression and Regression of Cisplatin Induced AKI [scRNA-seq]

Project description:Macrophages (MФs) play an important role in the repairment of acute kidney injury (AKI). The heterogeneity of renal MФ subsets during pathogenesis of AKI are still remain elusive. We used single cell RNA sequencing (scRNA-seq) to analyze the heterogeneity of renal MФs

2025-08-21 | GSE220675 | GEO

Transcriptome analysis of kidneys of cisplatin-induced AKI model

Project description:This study was aimed to investigate the role and underlying mechanism of TRPM2 in cisplatin nephrotoxicity. Cisplatin-induced acute kidney injury (AKI) model was established in WT and TRPM2-KO mice. The transcriptome profiling of the kidneys of WT and TRPM2-KO mice treated with cisplatin was compared to find differentially expressed gene which may be related to TRPM2 on cisplatin nephrotoxicity.

2023-03-30 | GSE203584 | GEO

Transcriptome analysis of kidneys of cisplatin (CP)-induced AKI model

Project description:In the cisplatin (CP)-induced AKI model group, the mice were administered CP and DXZ.

2023-07-30 | GSE200801 | GEO

FXR protects cisplatin-induced AKI via transcriptional regulation of ferroptosis.

Project description:Farnesoid X receptor (FXR, also known as NR1H4) is crucial to nephroprotective in several kinds of kidney diseases, including obesity, diabetes, aging, acute kidney injury and chronic kidney disease. FXR plays a key role in maintaining cholesterol and bile acid levels and is highly expressed in the liver, intestine and kidneys. In kidney diseases, it is reported that FXR has anti-lipogenic, anti‐inflammatory, antifibrotic, and antioxidant functions. Here, using genomics analysis, we investigated whether FXR attenuates cisplatin-induced AKI through the regulation of ferroptosis. The increased blood urea nitrogen, serum creatinine and ferroptotic responses in cisplatin-induced AKI mice were attenuated by treatment with FXR agonist, GW4064, while those were exacerbated in FXR knockout mice. Using RNA-sequencing analysis, we found novel target genes for FXR associated with ferroptosis. FXR agonist treatment increases lipid and glutathione metabolic gene expression and decreases cell death genes expression. This study identifies transcriptional regulation of ferroptosis by FXR as a potential therapeutic target for cisplatin-induced AKI.

2022-07-06 | GSE193860 | GEO

Transcriptome analysis of kidneys of cisplatin-induced AKI model

Project description:Transcriptome analysis of kidneys of cisplatin-induced AKI model

| PRJNA841498 | ENA

Time‑course analysis of cisplatin induced AKI in preclinical models: implications for testing different sources of MSCs

Project description:Cisplatin remains the most effective and widely used treatment option for solid tumors, however, it is also responsible for 30 - 46% incidence of AKI in cancer patients. Thus, despite its broad anti-cancer potential, clinical use of this chemotherapeutic agent remains constrained. In the last decade, mesenchymal stem cells (MSCs) have been proposed as a potentially useful therapeutic strategy in various diseases, including AKI, given their ability to reduce apoptosis and accelerate tubular cell regeneration. In the present study, we looked at the dose dependent response to cisplatin in two different mouse strains, CD1 and C57BL/6 mice, and performed a transcriptome based time-series analysis of the molecular signature in both male and female mice during progression of cisplatin-induced AKI, in order to generate a robust and reproducible pre-clinical model with the proposed aim to investigate the ability of MSCs from three different sources (adult and neonatal) as a rescue therapy to reverse kidney injury.

2024-05-31 | GSE263678 | GEO

Kidney Single-Cell Atlas Reveals Macrophage Heterogeneity in Progression and Regression of Cisplatin Induced AKI.

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-08-20 | GSE220691 | GEO

Transcriptome analysis of kidneys of cisplatin (CP)-induced AKI model

Project description:Transcriptome analysis of kidneys of cisplatin (CP)-induced AKI model

| PRJNA826849 | ENA

Proteomic analysis of cisplatin exposure on the kidney cortex proteome and the effect of preconditioning

Project description:Acute kidney injury and nephrotoxicity are important clinical side effects of cisplatin. Thus, the mechanisms of this disease, and potential treatment options are important to understand in their entity. Here, we analyzed the proteome of cisplatin induced acute kidney injury in a mouse model. Functionally we found that calorie restriction was able to completely blunt Cisplatin induced AKI, and hypoxia ameliorated cCisplatin induced AKI. To investigate the mechanism for this in high throughput, we performed label-free single-shot proteomic analyses of these kidneys.Acute kidney injury and nephrotoxicity are important clinical side effects of cisplatin. Thus, the mechanisms of this disease, and potential treatment options are important to understand in their entity. Here, we analyzed the proteome of cisplatin induced acute kidney injury in a mouse model. Functionally we found that calorie restriction was able to completely blunt Cisplatin induced AKI, and hypoxia ameliorated cCisplatin induced AKI. To investigate the mechanism for this in high throughput, we performed label-free single-shot proteomic analyses of these kidneys.

2020-01-30 | PXD005525 | Pride

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