Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis

ABSTRACT: Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis

PROVIDER: PRJNA1234150 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR32635400_1.fastq.gz	Fastqsanger.gz
	SRR32635400_2.fastq.gz	Fastqsanger.gz
	SRR32635401_1.fastq.gz	Fastqsanger.gz
	SRR32635401_2.fastq.gz	Fastqsanger.gz
	SRR32635402_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis

Project description:This study aimed to investigate impact of myeloid ferritin heavy chain (FtH) deletion on iron trafficking in kidney health and disease. Myeloid FtH deletion (FtHΔ/Δ) led to upregulation of synuclein-α (Snca) as the only iron-binding protein. When exposed to kidney injury, FtHΔ/Δ mice exhibited significantly worse kidney function. Transcriptome analysis identified ferroptosis as a key pathway triggered by FtH deletion. This was confirmed by elevated expression of ferroptosis-related genes, oxidative stress markers, and increased iron deposition in the kidneys. The latter was mediated via reprogramming of macrophages to an iron-recycling phenotype by inducing Spic. Mechanistically, we demonstrate ferrireductase activity of monomeric Snca acts as a catalyst triggering oxidative stress and ferroptosis. Moreover, kidney accumulation of Snca is promoted in kidney diseases marked by heavy leukocyte infiltration in both mice and humans. These findings emphasize role of FtH in regulating iron metabolism and promoting kidney repair by suppressing Snca and Spic.

2025-03-17 | GSE291562 | GEO

Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis [Baseline WT-KO]

Project description:Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis [Baseline WT-KO]

| PRJNA1237842 | ENA

Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis [Fe treatment WT-KO]

Project description:Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis [Fe treatment WT-KO]

| PRJNA1228621 | ENA

Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis [Baseline WT-KO]

Project description:To investigate impact of myeloid ferritin heavy chain (FtH) deletion in kidney iron metabolism under baseline conditions, we performed bulk RNA sequencing on kidney tissues from FtHfl/fl (wild-type) and FtHΔ/Δ (myeloid-specific FtH-deficient) mice.

2025-03-23 | GSE292295 | GEO

Myeloid FtH deficiency accelerates kidney disease by inducing Snca and ferroptosis [Fe treatment WT-KO]

Project description:Following kidney injury, we observed increased iron depsoition in kidneys of myeloid specific FtH deficient (FtHΔ/Δ) mice when compared to wild-type (FtHfl/fl) kidneys. To explore mechanisms coordinating increased iron accumulation in FtHΔ/Δ kidneys, we employed a parenterally induced iron overload model by injecting 10–12-week-old male FtHfl/fl (wild-type) and FtHΔ/Δ (myeloid-specific FtH-deficient) mice with 0.4 mg/g body weight iron dextran via five intraperitoneal injections on consecutive days. Three days after the final injection, kidneys were harvested and sent for bulk RNA sequencing to assess transcriptional changes underlying tissue iron deposition due to FtH deletion in myeloid cells.

2025-03-17 | GSE290560 | GEO

Gene expression analysis in lungs of Mtb infected Fth+/+ and Fth-/- mice by employing RNA-Seq

Project description:Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study is to compare gene expression (RNA-seq) profile between Mtb infected Fth+/+ and Fth-/- mice at 9 weeks post Mtb infection. Gene expression analysis demonstrated an essential role for FtH in mitochondrial function and maintenance of central intermediary metabolism in vivo

2018-09-01 | GSE112361 | GEO

Transcriptional profiling of Treg cells obtained from lymph nodes of Foxp3GFP-Fth∆/∆ and control Foxp3GFP-Fth∆/∆ mice

Project description:To gain further mechanistic insight on how ferritin H chain (FTH) impacts TREG cell lineage maintenance.

2023-04-30 | GSE173181 | GEO

Transcriptome profiling of blood leukocytes from FtH LysM-/- and FtH fl/fl mice following sham or CLP surgery

Project description:Despite the prevalence and recognition of its detrimental impact, clinical complications of sepsis remain a major challenge. Here, we investigated the effects of myeloid ferritin heavy chain (FtH) in regulating the pathogenic sequelae of sepsis. We demonstrate that deletion of myeloid FtH leads to tolerance towards sepsis as evidenced by reduced serum cytokine levels, multi-organ dysfunction and subsequent mortality. We identified that such tolerance is predominantly mediated by the compensatory increase in circulating ferritin (ferritin light chain; FtL) in the absence of myeloid FtH. Our in vitro and in vivo studies indicate that prior exposure to ferritin provides significant tolerance to the septic process by restraining an otherwise dysregulated response to infection. These findings are mediated by an inhibitory action of ferritin on NF-κB activation and its downstream effects. Taken together, our findings suggest an essential immunomodulatory function for circulating ferritin and enhances our understanding of this acute phase reactant.

2019-02-26 | GSE114078 | GEO

Ageing in space: microgravity triggers ferroptosis and accelerates senescence in osteoblastic cells

Project description:Ageing in space: microgravity triggers ferroptosis and accelerates senescence in osteoblastic cells

| PRJNA932730 | ENA

ATF4 suppresses hepatocarcinogenesis by inducing SLC7A11 (xCT) to suppress stress-related ferroptosis

Project description:ATF4 suppresses hepatocarcinogenesis by inducing SLC7A11 (xCT) to suppress stress-related ferroptosis

| PRJNA789791 | ENA