Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Membrane phospholipid remodeling modulates nonalcoholic steatohepatitis progression by regulating mitochondrial homeostasis.

ABSTRACT: Membrane phospholipid remodeling modulates nonalcoholic steatohepatitis progression by regulating mitochondrial homeostasis.

PROVIDER: PRJNA902270 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22309733.fastq.gz	Fastqsanger.gz
	SRR22309734.fastq.gz	Fastqsanger.gz
	SRR22309735.fastq.gz	Fastqsanger.gz
	SRR22309736.fastq.gz	Fastqsanger.gz
	SRR22309737.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

Membrane phospholipid remodeling modulates nonalcoholic steatohepatitis progression by regulating mitochondrial homeostasis [Lpcat3_OE]

Project description:Nonalcoholic steatohepatitis (NASH), characterized by inflammation and fibrosis, is emerging as a leading etiology of hepatocellular carcinoma (HCC). However, the mechanisms underlying the pathogenesis of NASH are not well understood. Here, we show that membrane phospholipid (PL) composition determined by a remodeling process modulates the progression of NASH. The expression of lysophosphatidylcholine acyltransferase 3 (LPCAT3), a PL remodeling enzyme that produces polyunsaturated PLs, is dramatically suppressed in human NASH livers compared to controls. LPCAT3 expression is inversely correlated with NAFLD activity score and fibrosis stage. Loss of Lpcat3 in mouse liver promotes the development of both spontaneous and diet-induced NASH/HCC. Mechanistically, Lpcat3 deficiency increases reactive oxygen species production, likely due to impaired mitochondrial homeostasis as demonstrated by reduced mitochondrial DNA content and fragmented mitochondrial morphology. Overexpressing Lpcat3 in the liver ameliorates inflammation and fibrosis of NASH. These results suggest that manipulating LPCAT3 expression may be an effective therapeutic strategy for NASH.

2024-06-05 | GSE218074 | GEO

Membrane phospholipid remodeling modulates nonalcoholic steatohepatitis progression by regulating mitochondrial homeostasis [LKO_NASH]

2024-06-05 | GSE218073 | GEO

Membrane phospholipid remodeling modulates nonalcoholic steatohepatitis progression by regulating mitochondrial homeostasis [LKO_NASH]

Project description:Membrane phospholipid remodeling modulates nonalcoholic steatohepatitis progression by regulating mitochondrial homeostasis [LKO_NASH]

| PRJNA902276 | ENA

Membrane phospholipid remodeling modulates nonalcoholic steatohepatitis progression by regulating mitochondrial homeostasis [Lpcat3_OE]

Project description:Membrane phospholipid remodeling modulates nonalcoholic steatohepatitis progression by regulating mitochondrial homeostasis [Lpcat3_OE]

| PRJNA902275 | ENA

Membrane phospholipid remodeling modulates nonalcoholic steatohepatitis progression by regulating mitochondrial homeostasis.

Project description:Background and aims: NASH, characterized by inflammation and fibrosis, is emerging as a leading etiology of HCC. Lipidomics analyses in the liver have shown that the levels of polyunsaturated phosphatidylcholine (PC) are decreased in patients with NASH, but the roles of membrane PC composition in the pathogenesis of NASH have not been investigated. Lysophosphatidylcholine acyltransferase 3 (LPCAT3), a phospholipid (PL) remodeling enzyme that produces polyunsaturated PLs, is a major determinant of membrane PC content in the liver. Approach and results: The expression of LPCAT3 and the correlation between its expression and NASH severity were analyzed in human patient samples. We examined the effect of Lpcat3 deficiency on NASH progression using Lpcat3 liver-specific knockout (LKO) mice. RNA sequencing, lipidomics, and metabolomics were performed in liver samples. Primary hepatocytes and hepatic cell lines were used for in vitro analyses. We showed that LPCAT3 was dramatically suppressed in human NASH livers, and its expression was inversely correlated with NAFLD activity score and fibrosis stage. Loss of Lpcat3 in mouse liver promotes both spontaneous and diet-induced NASH/HCC. Mechanistically, Lpcat3 deficiency enhances reactive oxygen species production due to impaired mitochondrial homeostasis. Loss of Lpcat3 increases inner mitochondrial membrane PL saturation and elevates stress-induced autophagy, resulting in reduced mitochondrial content and increased fragmentation. Furthermore, overexpression of Lpcat3 in the liver ameliorates inflammation and fibrosis of NASH. Conclusions: These results demonstrate that membrane PL composition modulates the progression of NASH and that manipulating LPCAT3 expression could be an effective therapeutic for NASH.

2024-06-05 | GSE218075 | GEO

Nonalcoholic steatohepatitis in adolescents undergoing bariatric surgery

Project description:The genomic landscape of hepatic tissue affected by nonalcoholic steatohepatitis (NASH) in severely obese adolescents undergoing bariatric surgery is unknown. Our purpose here was to uncover genomic profiles of obese controls, and obese cases with nonalcoholic fatty liver disease (NAFLD), borderline nonalcoholic steatohepatitis, and definite nonalcoholic steatohepatitis, in order to clarify molecular functions, biological processes, and pathways that are dysregulated in nonalcoholic steatohepatitis in the severely obese adolescent. In a prospective observational cohort study, we have intra-operatively obtained 165 liver samples; of these 67 were submited for microarray analysis. Through ANOVA, we found 8648 genes with differential regulation between the four histologies; from these, we uncovered gene signatures shared between borderline and definite nonalcoholic steatohepatitis, and gene sets with differential effects between borderline and definite.

2017-07-21 | GSE66676 | GEO

Myeloid FoxO1 in Nonalcoholic Steatohepatitis

Project description:Myeloid FoxO1 in Nonalcoholic Steatohepatitis

| PRJNA839093 | ENA

AGXT overexpression during nonalcoholic steatohepatitis in mice

Project description:To investigate the effects of AAV8-mediated overexpression of AGXT in mice with diet-induced nonalcoholic steatohepatitis compared to AAV8-GFP

2023-02-19 | GSE224097 | GEO

Nonalcoholic fatty liver, but not nonalcoholic steatohepatitis is a protective factor to tetrachloroethylene-associated kidney effects in male C57BL/6J mice

Project description:Purpose: We investigated the tetrachloroethylene associated changes in kidney transcriptomes among healthy mice, nonalcoholic fatty liver disease mice, and nonalcoholic steatohepatitis mice.

2019-02-13 | GSE115641 | GEO

AGXT overexpression during nonalcoholic steatohepatitis in mice

Project description:AGXT overexpression during nonalcoholic steatohepatitis in mice

| PRJNA929896 | ENA