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Semaglutide ameliorates cardiac remodeling in male mice by optimizing energy substrate utilization through the Creb5/NR4a1 axis

ABSTRACT: Semaglutide ameliorates cardiac remodeling in male mice by optimizing energy substrate utilization through the Creb5/NR4a1 axis

PROVIDER: PRJNA1090397 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28406300_1.fastq.gz	Fastqsanger.gz
	SRR28406300_2.fastq.gz	Fastqsanger.gz
	SRR28406280_1.fastq.gz	Fastqsanger.gz
	SRR28406280_2.fastq.gz	Fastqsanger.gz
	SRR28406281_1.fastq.gz	Fastqsanger.gz

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Semaglutide ameliorates cardiac remodeling in male mice by optimizing energy substrate utilization through the Creb5/NR4a1 axis

Project description:Semaglutide, a glucagon-like peptide-1 receptor agonist, is clinically used as a glucose-lowering and weight loss medication due to its effects on energy metabolism. In heart failure, energy production is impaired due to altered mitochondrial function and increased glycolysis. However, the impact of semaglutide on cardiomyocyte metabolism under pressure overload remains unclear. Here we demonstrate that semaglutide improves cardiac function and reduces hypertrophy and fibrosis in a mouse model of pressure overload-induced heart failure. Semaglutide preserves mitochondrial structure and function under chronic stress. Metabolomics reveals that semaglutide reduces mitochondrial damage, lipid accumulation, and ATP deficiency by promoting pyruvate entry into the tricarboxylic acid cycle and increasing fatty acid oxidation. Transcriptional analysis shows that semaglutide regulates myocardial energy metabolism through the Creb5/NR4a1 axis in the PI3K/AKT pathway, reducing NR4a1 expression and its translocation to mitochondria. NR4a1 knockdown ameliorates mitochondrial dysfunction and abnormal glucose and lipid metabolism in the heart. These findings suggest that semaglutide may be a therapeutic agent for improving cardiac remodeling by modulating energy metabolism.

2024-03-26 | GSE262105 | GEO

Semaglutide ameliorates cardiac remodeling by optimizing energy substrate utilization and through the Creb5/NR4a1 axis in male mice

Project description:Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, RP China Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, RP China

2024-03-26 | MSV000094408 | MassIVE

GNPS - Semaglutide ameliorates cardiac remodeling by optimizing energy substrate utilization and through the Creb5/NR4a1 axis in male mice

Project description:Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, RP China Hubei Key Laboratory of Metabolic and Chronic Diseases, Wuhan, RP China

2024-03-26 | MSV000094408 | GNPS

Semaglutide Attenuates Neuroinflammation in Mice

Project description:Single-nucleus RNA sequencing (snRNA-seq) of the hippocampus and dorsal vagal complex (DVC) from mice treated with semaglutide or vehicle control prior to lipopolysaccharide (LPS)-induced neuroinflammation.

2026-05-20 | E-MTAB-16829 | biostudies-arrayexpress

Creb5 controls its own expression and directly induces the joint-interzone regulatory program [CutandRun_Sox9_GFP]

Project description:Our prior work indicated that the transcription factor Creb5 plays a crucial role in the genesis of synovial joints. Here, we perform an integrative analysis of the transcriptome, chromatin accessibility, and Creb5-chromatin occupancy in Creb5-expressing synovial joint progenitor cells. This analysis revealed that Creb5 directly binds to both its own two promoters and to the regulatory regions of the early joint markers, Gdf5 and Sfrp2; each of whose expression in the joint-interzone is Creb5-dependent. Functional enhancer analysis indicated that Creb5 binding sites in its own two promoters are necessary for these sequences to drive transgene expression in a pattern that mimics endogenous Creb5 expression. While Creb5 directly regulates both Gdf5 and Sfrp2 expression in the inner joint-interzone by binding to either CREs or TREs in their regulatory elements, Creb5 activates Barx1 expression specifically in the outer joint-interzone; and thus initiates both the formation of the joint-interzone and regionalization of cell fates within this tissue.

2025-06-05 | GSE281189 | GEO

Creb5 controls its own expression and directly induces the joint-interzone regulatory program [ATACseq_Sox9_GFP]

2025-06-05 | GSE281188 | GEO

Creb5 controls its own expression and directly induces the joint-interzone regulatory program [ATACseq_Prx1]

2025-06-05 | GSE281187 | GEO

Creb5 controls its own expression and directly induces the joint-interzone regulatory program [RNAseq_Sox9_GFP]

2025-06-05 | GSE281191 | GEO

Creb5 controls its own expression and directly induces the joint-interzone regulatory program [RNAseq_Prx1]

2025-06-05 | GSE281190 | GEO

Semaglutide targets mitochondria to regulate metabolism and inflammation in sarcopenia and osteoarthritis

Project description:Metabolic and inflammatory diseases often coexist, and become important challenges facing global health. As a traditional anti-obesity drug, semaglutide is reported to have therapeutic effects in sarcopenia and osteoarthritis (OA), but its mechanism of action still needs to be explored. Here we employed single-cell sequencing analysis to analyze transcriptome changes cross various tissues of high-fat diet (HFD) and OA model mice, and found that semaglutide significantly improved the metabolic and inflammatory disorders of muscle tissue during HFD and OA. Mechanistically, we found that semaglutide could enhance muscle mitochondrial metabolism and mitophagy, alleviated the activation of inflammatory cytokines caused by hypoxia, and regulated the progression of sarcopenia and OA across tissues. Intramuscular injection of mitochondria, pre-stimulated by semaglutide, could significantly alleviate OA inflammation and pain symptoms. These findings reveal the mitochondrial regulatory mechanism in the muscle-OA axis and provide a new perspective for the application of semaglutide in OA treatment.

2026-05-06 | PXD073074 | Pride

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