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Liver TET1 promotes metabolic dysfunction-associated steatotic liver disease

ABSTRACT: Liver TET1 promotes metabolic dysfunction-associated steatotic liver disease

PROVIDER: PRJNA1209064 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31956520_1.fastq.gz	Fastqsanger.gz
	SRR31956520_2.fastq.gz	Fastqsanger.gz
	SRR31956521_1.fastq.gz	Fastqsanger.gz
	SRR31956521_2.fastq.gz	Fastqsanger.gz
	SRR31956522_1.fastq.gz	Fastqsanger.gz

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Liver TET1 promotes metabolic dysfunction-associated steatotic liver disease

Project description:DNA demethylation is regulated by the TET family proteins, whose enzymatic activity requires 2-oxoglutarate (2-OG) and iron that both are elevated in MASLD. We aimed to investigate liver TET1 in MASLD progression. Depleting TET1 substantially alleviated MASLD progression. Whole body Knockout of TET1 (TKO) slightly improved diet induced obesity and glucose homeostasis. Intriguingly, hepatic cholesterols, triglycerides, were significantly decreased upon TET1 depletion. Moreover, targeting TET1 with a small molecule inhibitor significantly suppressed MASLD progression. Liver TET1 plays a deleterious role in MASLD, suggesting the potential of targeting TET1 in hepatocytes to suppress MASLD.

2025-03-04 | GSE286394 | GEO

Oxidised apolipoprotein peptidome characterise metabolic dysfunction-associated steatotic liver disease.Oxidised apolipoprotein peptidome characterise metabolic dysfunction-associated steatotic liver disease.

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Deep proteome profiling of metabolic dysfunction-associated steatotic liver disease

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Hepatic miR-93 promotes the pathogenesis of metabolic dysfunction-associated steatotic liver disease by suppressing SIRT1

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Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent hepatic disorder worldwide and closely associated with type 2 diabetes mellitus (T2DM). The pathogenesis of MASLD is multifaceted and its treatment options are very limited. Consequently, it is urgent to identify novel therapeutic targets and develop effective treatment strategies. RNA sequencing analysis was performed to understand the transcriptomic changes in a mouse model of MASLD.

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Untargeted proteomic analysis of simultaneously collected human liver tissue and plasma of patients with a histological diagnosis of metabolic dysfunction-associated steatotic liver disease.

Project description:The liver tissue and plasma were collected from patients when undergoing liver biopsy for a diagnosis of metabolic dysfunction-associated steatotic liver disease (MASLD), along with controls who had no histological abnormalities. The study group included seven patients with no liver histological abnormalities and 64 patients with MASLD across its spectrum, including those with metabolic dysfunction-associated steatotic hepatitis (MASH) and those with cirrhosis. The data were compared between liver tissue and plasma, across various stages of MASLD, and for the detection of biomarkers for different stages of MASLD.

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Aging Promotes Metabolic Dysfunction-Associated Steatotic Liver Disease by Inducing Ferroptotic Stress

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Liver-Targeted siRNA Therapy Reveals a Causal Role of Metabolic Dysfunction-Associated Steatotic Liver Disease in Brain Dysfunction

Project description:Metabolic-dysfunction-associated steatotic liver disease (MASLD) has traditionally been studied as a liver-centric condition. However, growing clinical and experimental evidence reveals a strong link between MASLD and cognitive impairment and sensorimotor alterations. The mechanisms underlying this liver-brain axis remain poorly defined, and whether hepatic dysfunction alone is sufficient to drive central nervous system deficits is unclear. Using diet-induced non-obese mouse models of MASLD, we performed comprehensive neurocognitive and behavioral assessments. MASLD was associated with marked alterations in social memory, sensorimotor processing, and hippocampal function, including decreased parvalbumin-positive interneurons, reduced dendritic spine density, and diminished indicators of neurogenesis in the hippocampal dentate gyrus. Then, we selectively modulated liver metabolism through a hepatocyte-targeted siRNA therapy against Cyclin M4 (CNNM4), a magnesium transporter dysregulated in MASLD, employing GalNAc-siRNA technology for targeted delivery. Notably, liver-specific intervention with siRNA-CNNM4 reversed features of impaired social memory and sensorimotor processing through recovery of hippocampal synaptogenesis and mitochondrial function pathways, alongside activation of neurogenesis-associated transcriptional programs. Our findings demonstrate that liver pathology is sufficient to drive neurobehavioral and hippocampal dysfunction in MASLD. Importantly, hepatic-specific intervention restores brain function, strongly supporting the existence of a causal and therapeutically targetable liver-brain axis. These results open new avenues for treating MASLD-associated neurological complications through liver-directed therapies.

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Targeting Senescent Hepatocytes for Treatment of Metabolic Dysfunction-associated Steatotic Liver Disease and Multi-organ Dysfunction

Project description:Senescent hepatocytes accumulate in metabolic dysfunction-associated steatotic liver disease (MASLD) and are linked to worse clinical outcomes. However, their heterogeneity and lack of specific markers have made them difficult to target therapeutically. Here, we define a senescent hepatocyte gene signature (SHGS) using in vitro and in vivo models and show that it tracks with MASLD progression/regression across mouse models and large human cohorts. Single-nucleus RNA-sequencing and functional studies reveal that SHGS+ hepatocytes originate from p21+ cells, lose key liver functions and release factors that drive disease progression. One such factor, GDF15, increases in circulation alongside SHGS+ burden and disease progression. Through chemical screening, we identify senolytics that selectively eliminate SHGS+ hepatocytes and improve MASLD in mice. Notably, SHGS enrichment also correlates with dysfunction in other organs. These findings establish SHGS+ hepatocytes as key drivers of MASLD and highlight a potential therapeutic strategy for targeting senescent cells in liver disease and beyond.

2025-02-21 | GSE288534 | GEO

Metabolic dysfunction-associated steatotic liver disease may increase intrahepatic interferon gene signatures in patients with chronic hepatitis B

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