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PAD4 deletion inhibited obstruction-induced kidney inflammation and fibrosis

ABSTRACT: PAD4 deletion inhibited obstruction-induced kidney inflammation and fibrosis

PROVIDER: PRJNA1136535 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29848789_1.fastq.gz	Fastqsanger.gz
	SRR29848789_2.fastq.gz	Fastqsanger.gz
	SRR29848790_1.fastq.gz	Fastqsanger.gz
	SRR29848790_2.fastq.gz	Fastqsanger.gz
	SRR29848791_1.fastq.gz	Fastqsanger.gz

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PAD4 deletion inhibited obstruction-induced kidney inflammation and fibrosis

Project description:To understand the roles and mechanisms of neutrophil extracellular traps (NETs) in unilateral ureteral obstruction (UUO)-induced renal fibrosis, we performed RNA sequencing of UUO kidneys from wild-type and PAD4-deficient mice. PAD4 deletion led to reduced expression of fibrosis- and injury-associated genes, as well as inflammatory cytokines in UUO kidneys. Enrichment analysis of the downregulated genes in PAD4-deficient mice revealed a drastic decrease in inflammation pathways, such as T cell-associated pathways and cytokine-cytokine receptor interaction.

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DMM inhibited obstruction-induced renal fibrosis by blunting inflammation and activating PPAR signaling

Project description:To understand the roles and mechanisms of DMM in unilateral ureteral obstruction (UUO)-induced renal fibrosis, we performed RNA sequencing of UUO kidneys from mice treated with or without dimethyl malonate (DMM). DMM administration led to metabolic reprogramming in obstructed kidneys, the genes associated with the metabolism of fatty acid, organic acid, cellular amino acid, and mitochondrial function were significantly upregulated. Conversely, the downregulated genes in DMM-treated mice were involved in inflammation, including T cell immunity. Moreover, the upregulated genes in DMM-treated mice were associated with PPAR signaling. The RNA-seq analysis suggests that DMM activated PPAR and metabolic pathways while inhibited inflammatory signalings.

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PAD4⁺ Neutrophils Promote Hepatic Stellate Cell Activation and Accelerate MASH Fibrosis Progression via NETs-DNA/TAOK1/MAPK Pathways

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