{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Fleischer S"],"funding":["American Heart Association","NIBIB NIH HHS","U.S. Department of Health & Human Services | NIH | National Institute of Biomedical Imaging and Bioengineering (NIBIB)","NHLBI NIH HHS","U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute","NCI NIH HHS","U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI)","American Heart Association (American Heart Association, Inc.)","U.S. Department of Health & Human Services | NIH | National Institute of Biomedical Imaging and Bioengineering"],"pagination":["1123-1139"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11399098"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["3(9)"],"pubmed_abstract":["Systemic lupus erythematosus (SLE) is a heterogenous autoimmune disease that affects multiple organs, including the heart. The mechanisms of myocardial injury in SLE remain poorly understood. In this study, we engineered human cardiac tissues and cultured them with IgG from patients with SLE, with and without myocardial involvement. IgG from patients with elevated myocardial inflammation exhibited increased binding to apoptotic cells within cardiac tissues subjected to stress, whereas IgG from patients with systolic dysfunction exhibited enhanced binding to the surface of live cardiomyocytes. Functional assays and RNA sequencing revealed that, in the absence of immune cells, IgG from patients with systolic dysfunction altered cellular composition, respiration and calcium handling. Phage im"],"journal":["Nature cardiovascular research"],"pubmed_title":["An engineered human cardiac tissue model reveals contributions of systemic lupus erythematosus autoantibodies to myocardial injury."],"pmcid":["PMC11399098"],"funding_grant_id":["19TPA34910217","P41 EB027062","P41EB027062","3R01HL076485","P30 CA013696","R01 HL076485"],"pubmed_authors":["Whitehead J","Venturini G","Nash TR","Morsink M","Liberman M","Tavakol DN","Graney PL","Fleischer S","Lock RI","Friedman RA","Soni RK","Zhuang RZ","Tamargo MA","Lamberti MJ","Seidman JG","Vunjak-Novakovic G","Winchester R","Seidman CE","Li V","Kim Y","Geraldino-Pardilla L"],"additional_accession":[]},"is_claimable":false,"name":"An engineered human cardiac tissue model reveals contributions of systemic lupus erythematosus autoantibodies to myocardial injury.","description":"Systemic lupus erythematosus (SLE) is a heterogenous autoimmune disease that affects multiple organs, including the heart. The mechanisms of myocardial injury in SLE remain poorly understood. In this study, we engineered human cardiac tissues and cultured them with IgG from patients with SLE, with and without myocardial involvement. IgG from patients with elevated myocardial inflammation exhibited increased binding to apoptotic cells within cardiac tissues subjected to stress, whereas IgG from patients with systolic dysfunction exhibited enhanced binding to the surface of live cardiomyocytes. Functional assays and RNA sequencing revealed that, in the absence of immune cells, IgG from patients with systolic dysfunction altered cellular composition, respiration and calcium handling. Phage im","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Sep","modification":"2026-06-02T11:48:38.097Z","creation":"2025-04-04T09:49:11.354Z"},"accession":"S-EPMC11399098","cross_references":{"pubmed":["39195859"],"doi":["10.1038/s44161-024-00525-w"]}}