{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["56(6)"],"submitter":["Heng Y"],"pubmed_abstract":["Diabetes accelerates vascular senescence, which is the basis for atherosclerosis and stiffness. The activation of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and oxidative stress are closely associated with progressive senescence in vascular smooth muscle cells (VSMCs). The vascular protective effect of FGF21 has gradually gained increasing attention, but its role in diabetes-induced vascular senescence needs further investigation. In this study, diabetic mice and primary VSMCs are transfected with an FGF21 activation plasmid and treated with a peroxisome proliferator-activated receptor γ (PPARγ) agonist (rosiglitazone), an NLRP3 inhibitor (MCC950), and a spleen tyrosine kinase (SYK)-specific inhibitor, R406, to detect senescence-associated markers. We find "],"journal":["Acta biochimica et biophysica Sinica"],"pagination":["892-904"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11214975"],"repository":["biostudies-literature"],"pubmed_title":["FGF21 overexpression alleviates VSMC senescence in diabetic mice by modulating the SYK-NLRP3 inflammasome-PPARγ-catalase pathway."],"pmcid":["PMC11214975"],"pubmed_authors":["Liu H","Li H","Li J","Liang X","Yang B","Wei W","Wu F","Zhang P","Heng Y","Dong H","Fu J","Cheng L","Liu C"],"additional_accession":[]},"is_claimable":false,"name":"FGF21 overexpression alleviates VSMC senescence in diabetic mice by modulating the SYK-NLRP3 inflammasome-PPARγ-catalase pathway.","description":"Diabetes accelerates vascular senescence, which is the basis for atherosclerosis and stiffness. The activation of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and oxidative stress are closely associated with progressive senescence in vascular smooth muscle cells (VSMCs). The vascular protective effect of FGF21 has gradually gained increasing attention, but its role in diabetes-induced vascular senescence needs further investigation. In this study, diabetic mice and primary VSMCs are transfected with an FGF21 activation plasmid and treated with a peroxisome proliferator-activated receptor γ (PPARγ) agonist (rosiglitazone), an NLRP3 inhibitor (MCC950), and a spleen tyrosine kinase (SYK)-specific inhibitor, R406, to detect senescence-associated markers. We find ","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jun","modification":"2025-04-18T15:27:34.804Z","creation":"2025-04-07T02:09:13.189Z"},"accession":"S-EPMC11214975","cross_references":{"pubmed":["38733164"],"doi":["10.3724/abbs.2024032"]}}