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

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

PROVIDER: PRJNA1162804 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30723365_1.fastq.gz	Fastqsanger.gz
	SRR30723365_2.fastq.gz	Fastqsanger.gz
	SRR30723366_1.fastq.gz	Fastqsanger.gz
	SRR30723366_2.fastq.gz	Fastqsanger.gz
	SRR30723367_1.fastq.gz	Fastqsanger.gz

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

Project description:The molecular mechanisms underlying the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD) remain largely unclear. Emerging evidence suggests that microRNAs (miRNAs) play a critical role in transcriptional regulation by targeting genes involved in MASLD and other metabolic disorders, this study aims to elucidate the role of miR-93 in lipid metabolism and its impact on MASLD progression.

2025-04-14 | GSE277560 | GEO

Unraveling Diabetic Cardiomyopathy (DCM): The Critical Role of the Yap–miR-22-3p–Sirt1 axis in the Pathogenesis of DCM

Project description:Background: Diabetic cardiomyopathy (DCM), characterized by myocardial hypertrophy and myocardial fibrosis, is a severe complication of diabetes. Yes-associated protein (Yap) activation contributes to myocardial remodeling and cardiac dysfunction. This study investigated the role of Yap and its molecular mechanism in DCM. Methods: Yap expression was assessed in mice with type 2 diabetes mellitus (T2DM) and high glucose (HG) + insulin-treated neonatal rat cardiomyocytes (NRCMs). Adeno-associated virus transfection, siRNA transfection, and a transgenic mouse model were used to manipulate Yap and sirtuin 1 (Sirt1) expression in vivo and in vitro. RNA sequencing, differential gene analysis, and miRNA sequencing were used to identify downstream targets of Yap and the underlying mechanisms. Functional assays were used to evaluate cardiomyocyte hypertrophy and fibrosis through molecular markers, cell morphology, and echocardiography. Results: Yap expression was increased in HG + insulin-treated NRCMs and in the hearts of mice with T2DM, thereby promoting myocardial hypertrophy and fibrosis. Yap inhibition reduced the cardiomyocyte cross-sectional area, collagen deposition, and the levels of the hypertrophy markers atrial natriuretic peptide and β-myosin heavy chain. RNA sequencing identified Sirt1 as a downstream target of Yap. Bioinformatic analysis suggested that Yap positively regulates miR-22-3p, which inhibits Sirt1. Yap inhibition increased Sirt1 expression, mitigating myocardial remodeling. Conversely, Sirt1 knockdown reversed the protective effects of Yap inhibition, restoring hypertrophy and fibrosis. Conclusion: Yap promotes DCM progression by increasing miR-22-3p expression and suppressing Sirt1 expression. Targeting the Yap–miR-22-3p–Sirt1 axis might represent a novel therapeutic strategy for DCM, thereby improving myocardial structure and function.

2026-02-28 | GSE290303 | GEO

Renal tubular Sirt1 attenuates diabetic albuminuria by epigenetically suppressing Claudin-1 overexpression in podocytes.

Project description:We aim to investigate the role of renal Sirt1 on albuminuria. To further development of our gene expression approach to biodosimetry, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish between wild type(C57BL/6J) mice treated with streptozotocin (WT+STZ) and Sirt1-overexpressing transgenic mice treated with streptozotocin (TG+STZ) mice. To elucidate the molecular mechanisms underlying the amelioration of albuminuria by our TG (Sirt1-overexpressing transgenic) mice, we performed DNA microarray analysis using micro-dissected glomerular regions to examine the differences in gene expression between WT+STZ and TG+STZ mice.

2018-03-08 | GSE50140 | GEO

NMN protects cisplatin induced AKI via NAD+/SIRT1 pathway

Project description:Acute kidney injury (AKI) is a critical public health concern with high morbidity and mortality.Using male mice and HK-2 cells, we found that the NAD⁺ precursor NMN restored renal NAD⁺ levels and activated SIRT1, markedly lowering plasma creatinine and BUN, reducing NGAL and KIM-1 expression, suppressing IL-6/IL-18 and neutrophil infiltration, and attenuating ROS and LDH release. Thus, NMN protects against CIS-AKI via the NAD⁺–SIRT1 pathway and represents a promising therapeutic strategy.

2026-01-01 | GSE306603 | GEO

NSD2 aggravates metabolic dysfunction-associated steatotic liver disease progression by suppressing TFEB-mediated autophagy-lysosomal pathway

Project description:NSD2 aggravates metabolic dysfunction-associated steatotic liver disease progression by suppressing TFEB-mediated autophagy-lysosomal pathway

| PRJNA1213738 | ENA

Testing the contribution of FGL1 to the pathogenesis of metabolic dysfunction-associated steatotic liver disease and hepatocellular carcinoma

Project description:Metabolic dysfunction-associated steatotic liver disease (MASLD) begins with simple steatosis, which can progress to hepatocellular carcinoma (HCC). The pathogenesis of MASLD alters the secretion of hepatokines such as fibrinogen-like 1 (FGL1), a candidate mediator of liver steatosis and hyperglycemia. To investigate the contribution of FGL1 to liver diseases, we compared wild-type mice to mice with hepatocyte-specific deletion of Fgl1 subjected to a steatosis or HCC experimental protocol. We found that mice deficient for Fgl1 in hepatocytes showed higher levels of plasma glucose, pronounced metabolic alterations and liver injury when fed a western diet compared to their wild-type counterparts. However, both genotypes exhibited a similar lipid deposition in the liver. Similarly, wild type and Fgl1-deficient mice displayed comparable liver alterations during HCC progression. We observed that FGL1 expression was repressed during MASLD progression in mice and human concomitantly with the severity of liver injury. Altogether, these findings suggest that FGL1 is not a major contributor to the pathogenesis of MASLD and HCC.

2025-08-27 | GSE291163 | GEO

Convergence of SIRT1 and ATR signaling to modulate replication origin dormancy

Project description:SIRT1 chromatin interactome analysis was performed to identify SIRT1 molecular targets involved in replication initiation from cells containing either WT or H363Y SIRT1. Co-IP-MS of pT530 SIRT1 from chromatin extracts was performed. Files are: 1422 WT SIRT1 untreated U2OS; 1423 WT SIRT1 H2O2 treated, U2OS; 1424 H363Y SIRT1 untreated U2OS; 1425 H363Y SIRT1 H2O2 U2OS; 1426 KO SIRT1 untreated U2OS; 1427 KO SIRT1 H2O2 U2OS; 1428 WT SIRT1 untreated HEK; 1429 WT SIRT1 H2O2 HEK; 1430 WT SIRT1 untreated HCT116; 1431 WT SIRT1 H2O2 HCT116; 1432 WT SIRT1 untreated K562; 1433 WT SIRT1 H2O2 K562. Each sample has 9 fractions.

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SIRT1 activation attenuates microglia-mediated synaptic engulfment in postoperative cognitive

Project description:Background: Postoperative cognitive dysfunction (POCD) is a debilitating neurological complication in surgical patients. Current research has focused mainly on microglial activation, but less is known about the resultant neuronal synaptic changes. Recent studies have suggested that silent information regulator 1 (SIRT1) plays a critical role in several different neurological disorders via its involvement in microglial activation. In this study, we evaluate the effects of SIRT1 activation in a POCD mouse model. Methods: Exploratory laparotomy was performed in mice aged 12-14 months under sevoflurane anesthesia to establish our animal POCD model. Transcriptional changes in the hippocampus after anesthesia and surgery were evaluated by RNA sequencing. SIRT1 expression was verified by Western Blot. Mice were treated with SIRT1 agonist SRT1720 or vehicle after surgery. Changes in microglia morphology, microglial phagocytosis, presence of dystrophic neurites, and dendritic spine density were evaluated. Cognitive performance was evaluated using the Y maze and Morris water maze. Results: SIRT1 expression levels were downregulated in POCD. Exposure to anesthesia and surgery lead to alteration in microglia morphology, increased synaptic engulfment, dendritic spine loss, and cognitive deficits. These effects were alleviated by SRT1720 administration. Conclusion: This study suggests an important neuroprotective role for SIRT1 in POCD pathogenesis. Increasing SIRT1 function represents a promising therapeutic strategy for prevention and treatment of POCD.

2022-12-09 | GSE215410 | GEO

Sirt1 targeting promotes Treg function

Project description:Sirtuin-1 (Sirt1), a class III histone/protein deacetylase is central to cellular metabolism, stress responses and aging, but its contributions to various host immune functions have been little investigated. To study the role of Sirt1 in T-cell functions, we undertook targeted deletions by mating mice with a floxed Sirt1 gene to mice expressing CD4-cre or Foxp3-cre recombinase, respectively. We found that Sirt1 deletion left conventional T-effector cell activation, proliferation and cytokine production largely unaltered. However, Sirt1 targeting promoted the expression and acetylation of Foxp3, a key transcription factor in T-regulatory (Treg) cells, and increased Treg suppressive functions in vitro and in vivo. Consistent with these data, mice with targeted deletions of Sirt1 in either CD4+ T-cells or Foxp3+ Treg cells exhibited prolonged survival of MHC-mismatched cardiac allografts. Allografts in Sirt1 targeted recipients showed long-term preservation of myocardial histology and infiltration by Foxp3+ Treg cells. Comparable results were seen in wild-type allograft recipients treated with Sirt1 inhibitors, such as EX-527 and splitomicin. Hence, Sirt1 may inhibit Treg functions and its targeting may have therapeutic value in autoimmunity and transplantation.

2011-01-05 | GSE26425 | GEO

Streptomyces sp. 93 strain:93

Project description:Streptomyces sp. 93 strain:93 Genome sequencing

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