{"database":"iProX","file_versions":[],"scores":null,"additional":{"omics_type":["Proteomics"],"submitter":["Bin Feng"],"species":["Homo Sapiens"],"full_dataset_link":["http://www.iprox.org/page/project.html?id=IPX0005229000"],"submitter_email":["njufengbin@163.com"],"submitter_affiliation":["Department of Endocrinology and Metabolism, The First Affiliated Hospital of Soochow University"],"sample_protocol":[""],"repository":["iProX"],"data_protocol":[""],"pubmed_abstract":["<h4>Background</h4>Heart failure with preserved ejection fraction (HFpEF) is a common disease with high morbidity and lacks effective treatment. We investigated the protective effects of the long-term application of the sodium-glucose cotransporter 2 inhibitor (SGLT2i) dapagliflozin on diabetes-associated HFpEF in a rat model. Serum proteomics and metabolomics analysis were also conducted in type 2 diabetic patients with HFpEF treated with dapagliflozin.<h4>Methods</h4>Male Zucker diabetic fatty (ZDF) rats were used as a model of diabetic cardiomyopathy. From weeks 16 to 28, animals were given a vehicle or dapagliflozin (1 mg/kg) once daily. Primary blood biochemistry indices, echocardiography, histopathology, and cardiac hemodynamics were determined during the study period. The key markers of myocardial fibrosis, nitro-oxidative stress, inflammation, apoptosis, autophagy, and AMPK/mTOR signaling were examined. Additionally, healthy controls and individuals with type 2 diabetes were enrolled and 16 serum samples from 4 groups were randomly selected. Serum proteome and metabolome changes after dapagliflozin treatment were analyzed in diabetic individuals with HFpEF.<h4>Results</h4>Dapagliflozin effectively prevented the development of HFpEF in rats with diabetes by mitigating nitro-oxidative stress, pro-inflammatory cytokines, myocardial hypertrophy, and fibrosis, reducing apoptosis, and restoring autophagy through AMPK activating and mTOR pathway repressing. Proteomics and metabolomics revealed that cholesterol and high-density lipoprotein particle metabolism, nicotinate and nicotinamide metabolism, arginine biosynthesis, and cAMP and peroxisome proliferator-activated receptor (PPAR) signaling are the major disturbed pathways in HFpEF patients treated with dapagliflozin.<h4>Conclusion</h4>Long-term treatment with dapagliflozin significantly prevented the development of HFpEF in diabetic rats. Dapagliflozin could be a promising therapeutic strategy in managing HFpEF individuals with type 2 diabetes."],"pubmed_title":["Therapeutic effects on the development of heart failure with preserved ejection fraction by the sodium-glucose cotransporter 2 inhibitor dapagliflozin in type 2 diabetes."],"pubmed_authors":["Feng Bin B, Yu Peiran P, Yu Hao H, Qian Buyun B, Li Yuan Y, Sun Kangyun K, Shi Bimin B, Zhang Nannan N, Xu Guidong G"],"additional_accession":[]},"is_claimable":false,"name":"Serum proteomics of T2DM individuals with HFpEF after dapagliflozin treatment by tandem mass spectrometry","description":"A quantitative proteomic profiling by TMT was performed on serum of T2DM individuals with or without dapagliflozin treatment","dates":{"publication":"Tue Oct 18 00:00:00 BST 2022"},"accession":"PXD037538","cross_references":{"TAXONOMY":["9606"],"pubmed":["37386620"]}}