{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Sen P"],"funding":["Deutsche Forschungsgemeinschaft","DZHK","Friedrich-Baur-Stiftung","DZD"],"pagination":["93-112"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12804299"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["121(1)"],"pubmed_abstract":["Both diabetes mellitus (DM) and chronic kidney disease (CKD) predispose to cardiac remodeling and coronary microvascular dysfunction, which is proposed to be mediated through increased oxidative stress. To link oxidative stress and cardiac remodeling in DM and CKD, CKD was induced in genetically modified DM swine (INS<sup>C94Y</sup> transgenic) at 10-12 weeks of age via renal microembolization, while non-embolized DM and wild-type (WT) swine served as controls. Compared to WT, 1) DM animals displayed modest LV dilation and a slight decline in ejection fraction, with increased end-systolic pressures and coronary blood flow. Addition of CKD did not further aggravate these alterations, but increased the pressure and diastolic wall stress compared to WT. 2) Proteomic analysis revealed enrichme"],"journal":["Basic research in cardiology"],"pubmed_title":["From kidney injury to cardiac dysfunction: the central role of oxidative stress in diabetes and CKD."],"pmcid":["PMC12804299"],"funding_grant_id":["81X2600286","project # 453989101","SFB 1525","Ma 2528/9-2","DZHK81Z0600207","project #315254108","Reg Nr- 28/21","82DZD08D03","Ma 2528/8-1","project # 505805397"],"pubmed_authors":["Merkus D","Frohlich T","Bachter M","Zhang J","Bierschenk S","Ornek I","Nickel AG","Hamers J","Clauss S","Sen P","Stockl JB","Wolf E","Maack C","d'Ambrosio L","Renner S","Shashikadze B","Sittig T"],"additional_accession":[]},"is_claimable":false,"name":"From kidney injury to cardiac dysfunction: the central role of oxidative stress in diabetes and CKD.","description":"Both diabetes mellitus (DM) and chronic kidney disease (CKD) predispose to cardiac remodeling and coronary microvascular dysfunction, which is proposed to be mediated through increased oxidative stress. To link oxidative stress and cardiac remodeling in DM and CKD, CKD was induced in genetically modified DM swine (INS<sup>C94Y</sup> transgenic) at 10-12 weeks of age via renal microembolization, while non-embolized DM and wild-type (WT) swine served as controls. Compared to WT, 1) DM animals displayed modest LV dilation and a slight decline in ejection fraction, with increased end-systolic pressures and coronary blood flow. Addition of CKD did not further aggravate these alterations, but increased the pressure and diastolic wall stress compared to WT. 2) Proteomic analysis revealed enrichme","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Feb","modification":"2026-06-30T03:25:54.706Z","creation":"2026-06-30T03:21:09.521Z"},"accession":"S-EPMC12804299","cross_references":{"pubmed":["41419687"],"doi":["10.1007/s00395-025-01153-6"]}}