Glucagon-like peptide-1 receptor: mechanisms and advances in therapy

Signal Transduction and Targeted Therapy, Journal Year: 2024, Volume and Issue: 9(1)

Published: Sept. 18, 2024

The glucagon-like peptide-1 (GLP-1) receptor, known as GLP-1R, is a vital component of the G protein-coupled receptor (GPCR) family and found primarily on surfaces various cell types within human body. This specifically interacts with GLP-1, key hormone that plays an integral role in regulating blood glucose levels, lipid metabolism, several other crucial biological functions. In recent years, GLP-1 medications have become focal point medical community due to their innovative treatment mechanisms, significant therapeutic efficacy, broad development prospects. article thoroughly traces developmental milestones drugs, from initial discovery clinical application, detailing evolution diverse along distinct pharmacological properties. Additionally, this paper explores potential applications agonists (GLP-1RAs) fields such neuroprotection, anti-infection measures, reduction inflammation, enhancement cardiovascular function. It provides in-depth assessment effectiveness GLP-1RAs across multiple body systems-including nervous, cardiovascular, musculoskeletal, digestive systems. includes integrating latest trial data delving into signaling pathways mechanisms. primary goal emphasize extensive benefits using treating spectrum diseases, obesity, non-alcoholic fatty liver disease (NAFLD), neurodegenerative musculoskeletal forms cancer. ongoing new indications for drugs offers promising prospects further expanding interventions, showcasing field.

Language: Английский

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Unravelling the Role of PANoptosis in Liver Diseases: Mechanisms and Therapeutic Implications

Liver International, Journal Year: 2025, Volume and Issue: 45(4)

Published: March 21, 2025

PANoptosis is a multimodal form of cell death that involves inflammatory, apoptotic, and necroptotic pathways, playing key role in the development liver diseases. This article first outlines definition characteristics PANoptosis, then explores its mechanisms action different types diseases, including acute injury, failure, metabolic dysfunction-associated fatty disease, hepatocellular carcinoma. Furthermore, this analyses molecular regulatory network potential therapeutic targets. Finally, summarises current research on diseases future directions, it reviews emerging mechanism

Language: Английский

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Overexpression of DTX1 inhibits D-GalN/TNF-α-induced pyroptosis and inflammation in hepatocytes by regulating NLRP3 ubiquitination

Toxicology Research, Journal Year: 2024, Volume and Issue: 13(5)

Published: Sept. 2, 2024

Abstract Background Acute liver injury (ALI) is characterized by massive hepatocyte death and has high mortality poor prognosis. Hepatocyte pyroptosis plays a key role in the pathophysiology of ALI involved inflammatory response mediated NOD-like receptor protein 3 (NLRP3) inflammasome activation. Deltex 1 (DTX1) single transmembrane with ubiquitin E3 ligase activity closely cell growth, differentiation, apoptosis, as well intracellular signal transduction. However, little known about influence DTX1 on ALI. This study aimed to investigate inflammation induced D-galactosamine (D-GalN) tumor necrosis factoralpha (TNF-α) human hepatocytes (LO2 cells) vitro. Methods Cell was measured flow cytometry. The levels DTX1, pyroptosis-associated proteins, cytokines were detected quantitative real-time polymerase chain reaction, western blotting, enzyme-linked immunosorbent assay. Immunofluorescence staining, co-immunoprecipitation, ubiquitination, luciferase reporter chromatin immunoprecipitation assays performed detect regulation between NLRP3 or nuclear factor 4 alpha (HNF4α). Analysis variance compare groups. Results We found that decreased D-GalN/TNF-α-induced LO2 cells. overexpression significantly inhibited inflammation. interacted ubiquitination degradation. Furthermore, targeting NLRP3, knockdown In addition, HNF4α promoted transcription binding its promoter. Conclusion Our revealed suppressed regulating ubiquitination.

Language: Английский

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Bioinformatics combined with network pharmacology and experimental validation to identify key biomarkers of hepatocellular carcinoma and corresponding compounds in Radix Astragali and Pueraria Mirifica

Naunyn-Schmiedeberg s Archives of Pharmacology, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 16, 2024

Language: Английский

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Pyroptosis in Lung Cancer: The Emerging Role of Non-Coding RNAs

Pathology - Research and Practice, Journal Year: 2024, Volume and Issue: 263, P. 155619 - 155619

Published: Sept. 28, 2024

Language: Английский

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Trimethylamine Induced Chronic Kidney Injury by Activating the ZBP1-NLRP3 Inflammasome Pathway

Physiological Research, Journal Year: 2024, Volume and Issue: 5/2024, P. 779 - 789

Published: Nov. 8, 2024

Trimethylamine N-oxide (TMAO), a bioactive metabolite of gut microbes, plays pivotal role in the pathogenesis kidney diseases by activating programmed cell death (PCD) pathways. However, whether trimethylamine (TMA) contributes to chronic injury and which kind PCD is involved TMA-induced has not been previously evaluated. To observe effect TMA, male C57BL/6J mice were randomly divided into two groups: Control group TMA group. The intraperitoneally injected with 100 μmol/kg/day for three months, whereas normal saline same period. After plasma creatinine blood urea nitrogen levels, indicators function, increased significantly as compared those Furthermore, Masson staining assay showed that treatment led larger area fibrosis than did change Bax/Bcl-2 ratio, RIP1, RIP3 MLKL phosphorylation, or iron malondialdehyde levels tissues, indicating apoptosis, ferroptosis necroptosis injury. group, upregulated NLRP3, Caspase-1, IL-1β, cleaved-Caspase 8, Caspase-8, ZBP1 protein expression tissues. These results indicated ZBP1-NLRP3 inflammasome pathway was In conclusion, our studies revealed may take part progression induced

Language: Английский

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