Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: WMT improves patients with metabolic syndrome

PROVIDER: PRJNA881922 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR21688700.fastq.gz	Fastqsanger.gz
	SRR21688701.fastq.gz	Fastqsanger.gz
	SRR21688702.fastq.gz	Fastqsanger.gz
	SRR21688703.fastq.gz	Fastqsanger.gz
	SRR21688704.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 27

Similar Datasets

E-GEOD-46687

Project description:Gene Expression Profiling in 45X Turner Syndrome patients

2025-01-24 | E-GEOD-46687 | ExpressionAtlas

E-MTAB-3017

Project description:Peripheral blood gene expression profiles in obese subjects without metabolic syndrome.

2025-01-23 | E-MTAB-3017 | ExpressionAtlas

E-GEOD-63816

Project description:RNA-seq of bone marrow from patients with myelodysplastic syndrome

2025-01-24 | E-GEOD-63816 | ExpressionAtlas

E-MEXP-1956

Project description:Transcription profiling of cultured fibroblastic cell lines from Rett syndrome patients

2025-01-22 | E-MEXP-1956 | ExpressionAtlas

Project description:WHHPRO improves high fat diet induced metabolic syndrome in rats

| PRJNA988830 | ENA

E-GEOD-2461

Project description:Transcription profiling of mucosa from human patients with irritable bowel syndrome or ulcerative colitis

2025-01-24 | E-GEOD-2461 | ExpressionAtlas

NAD+ augmentation restores mitophagy and limits accelerated aging in Werner syndrome

Project description:Metabolic dysfunction is a primary feature of Werner syndrome (WS), a human premature aging disease caused by mutations in the gene encoding the Werner (WRN) DNA helicase. WS patients exhibit severe metabolic phenotypes, but the underlying mechanisms are not understood, and whether the metabolic deficit can be targeted for therapeutic intervention has not been determined. Here we report impaired mitophagy and depletion of NAD+, a fundamental ubiquitous molecule, in WS patient samples and WS invertebrate models. WRN regulates transcription of a key NAD+ biosynthetic enzyme nicotinamide nucleotide adenylyltransferase 1 (NMNAT1). NAD+ repletion restores NAD+ metabolic profiles and improves mitochondrial quality through DCT-1 and ULK-1-dependent mitophagy. At the organismal level, NAD+ repletion remarkably extends lifespan and delays accelerated aging, including stem cell dysfunction, in C. elegans and Drosophila melanogaster models of WS. Our findings suggest that accelerated aging in WRN syndrome is mediated by impaired mitochondrial function and mitophagy, and that bolstering cellular NAD+ levels counteracts WS phenotypes.

2020-01-13 | PXD015644 | Pride