Osteopontin Promotes Left Ventricular Diastolic Dysfunction Through a Mitochondrial Pathway
Patients with chronic kidney disease (CKD) and coincident heart failure with preserved ejection fraction (HFpEF) may constitute a distinct HFpEF phenotype. Osteopontin (OPN) is a biomarker of HFpEF and predictive of disease outcome. We recently reported that OPN blockade reversed hypertension, mitoc...
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| Published in | Journal of the American College of Cardiology Vol. 73; no. 21; pp. 2705 - 2718 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
04.06.2019
Elsevier Limited |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0735-1097 1558-3597 1558-3597 |
| DOI | 10.1016/j.jacc.2019.02.074 |
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| Abstract | Patients with chronic kidney disease (CKD) and coincident heart failure with preserved ejection fraction (HFpEF) may constitute a distinct HFpEF phenotype. Osteopontin (OPN) is a biomarker of HFpEF and predictive of disease outcome. We recently reported that OPN blockade reversed hypertension, mitochondrial dysfunction, and kidney failure in Col4a3−/− mice, a model of human Alport syndrome.
The purpose of this study was to identify potential OPN targets in biopsies of HF patients, healthy control subjects, and human induced pluripotent stem cell–derived cardiomyocytes (hiPS-CMs), and to characterize the cardiac phenotype of Col4a3−/− mice, relate this to HFpEF, and investigate possible causative roles for OPN in driving the cardiomyopathy.
OGDHL mRNA and protein were quantified in myocardial samples from patients with HFpEF, heart failure with reduced ejection fraction, and donor control subjects. OGDHL expression was quantified in hiPS-CMs treated with or without anti-OPN antibody. Cardiac parameters were evaluated in Col4a3−/− mice with and without global OPN knockout or AAV9-mediated delivery of 2-oxoglutarate dehydrogenase-like (Ogdhl) to the heart.
OGDHL mRNA and protein displayed abnormal abundances in cardiac biopsies of HFpEF (n = 17) compared with donor control subjects (n = 12; p < 0.01) or heart failure with reduced ejection fraction patients (n = 12; p < 0.05). Blockade of OPN in hiPS-CMs conferred increased OGDHL expression. Col4a3−/− mice demonstrated cardiomyopathy with similarities to HFpEF, including diastolic dysfunction, cardiac hypertrophy and fibrosis, pulmonary edema, and impaired mitochondrial function. The cardiomyopathy was ameliorated by Opn−/− coincident with improved renal function and increased expression of Ogdhl. Heart-specific overexpression of Ogdhl in Col4a3−/− mice also improved cardiac function and cardiomyocyte energy state.
Col4a3−/− mice present a model of HFpEF secondary to CKD wherein OPN and OGDHL are intermediates, and possibly therapeutic targets.
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| AbstractList | Patients with chronic kidney disease (CKD) and coincident heart failure with preserved ejection fraction (HFpEF) may constitute a distinct HFpEF phenotype. Osteopontin (OPN) is a biomarker of HFpEF and predictive of disease outcome. We recently reported that OPN blockade reversed hypertension, mitochondrial dysfunction, and kidney failure in Col4a3
mice, a model of human Alport syndrome.
The purpose of this study was to identify potential OPN targets in biopsies of HF patients, healthy control subjects, and human induced pluripotent stem cell-derived cardiomyocytes (hiPS-CMs), and to characterize the cardiac phenotype of Col4a3
mice, relate this to HFpEF, and investigate possible causative roles for OPN in driving the cardiomyopathy.
OGDHL mRNA and protein were quantified in myocardial samples from patients with HFpEF, heart failure with reduced ejection fraction, and donor control subjects. OGDHL expression was quantified in hiPS-CMs treated with or without anti-OPN antibody. Cardiac parameters were evaluated in Col4a3
mice with and without global OPN knockout or AAV9-mediated delivery of 2-oxoglutarate dehydrogenase-like (Ogdhl) to the heart.
OGDHL mRNA and protein displayed abnormal abundances in cardiac biopsies of HFpEF (n = 17) compared with donor control subjects (n = 12; p < 0.01) or heart failure with reduced ejection fraction patients (n = 12; p < 0.05). Blockade of OPN in hiPS-CMs conferred increased OGDHL expression. Col4a3
mice demonstrated cardiomyopathy with similarities to HFpEF, including diastolic dysfunction, cardiac hypertrophy and fibrosis, pulmonary edema, and impaired mitochondrial function. The cardiomyopathy was ameliorated by Opn
coincident with improved renal function and increased expression of Ogdhl. Heart-specific overexpression of Ogdhl in Col4a3
mice also improved cardiac function and cardiomyocyte energy state.
Col4a3
mice present a model of HFpEF secondary to CKD wherein OPN and OGDHL are intermediates, and possibly therapeutic targets. Patients with chronic kidney disease (CKD) and coincident heart failure with preserved ejection fraction (HFpEF) may constitute a distinct HFpEF phenotype. Osteopontin (OPN) is a biomarker of HFpEF and predictive of disease outcome. We recently reported that OPN blockade reversed hypertension, mitochondrial dysfunction, and kidney failure in Col4a3−/− mice, a model of human Alport syndrome. The purpose of this study was to identify potential OPN targets in biopsies of HF patients, healthy control subjects, and human induced pluripotent stem cell–derived cardiomyocytes (hiPS-CMs), and to characterize the cardiac phenotype of Col4a3−/− mice, relate this to HFpEF, and investigate possible causative roles for OPN in driving the cardiomyopathy. OGDHL mRNA and protein were quantified in myocardial samples from patients with HFpEF, heart failure with reduced ejection fraction, and donor control subjects. OGDHL expression was quantified in hiPS-CMs treated with or without anti-OPN antibody. Cardiac parameters were evaluated in Col4a3−/− mice with and without global OPN knockout or AAV9-mediated delivery of 2-oxoglutarate dehydrogenase-like (Ogdhl) to the heart. OGDHL mRNA and protein displayed abnormal abundances in cardiac biopsies of HFpEF (n = 17) compared with donor control subjects (n = 12; p < 0.01) or heart failure with reduced ejection fraction patients (n = 12; p < 0.05). Blockade of OPN in hiPS-CMs conferred increased OGDHL expression. Col4a3−/− mice demonstrated cardiomyopathy with similarities to HFpEF, including diastolic dysfunction, cardiac hypertrophy and fibrosis, pulmonary edema, and impaired mitochondrial function. The cardiomyopathy was ameliorated by Opn−/− coincident with improved renal function and increased expression of Ogdhl. Heart-specific overexpression of Ogdhl in Col4a3−/− mice also improved cardiac function and cardiomyocyte energy state. Col4a3−/− mice present a model of HFpEF secondary to CKD wherein OPN and OGDHL are intermediates, and possibly therapeutic targets. [Display omitted] Abnormal OGDHL expression was observed in cardiac biopsies of HFpEF patients compared to healthy donor or HFrEF groups. OGDHL levels were responsive to OPN activity in hiPS-CMs and rodent CMs. Cardiac structure and function analyses of Alport (Col4a3−/−) mice that model monogenic kidney disease revealed, in addition to hypertension and renal dysfunction, a HFpEF-like phenotype that included pulmonary edema, diastolic dysfunction, cardiac hypertrophy, myocardial fibrosis and mitochondrial dysfunction. We identify pivotal roles for OPN and mitochondrial OGDHL in the pathophysiology and show that cardiac-specific overexpression of Ogdhl alleviated cardiac dysfunction and improved energetics, similar to global OPN knockdown. Patients with chronic kidney disease (CKD) and coincident heart failure with preserved ejection fraction (HFpEF) may constitute a distinct HFpEF phenotype. Osteopontin (OPN) is a biomarker of HFpEF and predictive of disease outcome. We recently reported that OPN blockade reversed hypertension, mitochondrial dysfunction, and kidney failure in Col4a3-/- mice, a model of human Alport syndrome.BACKGROUNDPatients with chronic kidney disease (CKD) and coincident heart failure with preserved ejection fraction (HFpEF) may constitute a distinct HFpEF phenotype. Osteopontin (OPN) is a biomarker of HFpEF and predictive of disease outcome. We recently reported that OPN blockade reversed hypertension, mitochondrial dysfunction, and kidney failure in Col4a3-/- mice, a model of human Alport syndrome.The purpose of this study was to identify potential OPN targets in biopsies of HF patients, healthy control subjects, and human induced pluripotent stem cell-derived cardiomyocytes (hiPS-CMs), and to characterize the cardiac phenotype of Col4a3-/- mice, relate this to HFpEF, and investigate possible causative roles for OPN in driving the cardiomyopathy.OBJECTIVESThe purpose of this study was to identify potential OPN targets in biopsies of HF patients, healthy control subjects, and human induced pluripotent stem cell-derived cardiomyocytes (hiPS-CMs), and to characterize the cardiac phenotype of Col4a3-/- mice, relate this to HFpEF, and investigate possible causative roles for OPN in driving the cardiomyopathy.OGDHL mRNA and protein were quantified in myocardial samples from patients with HFpEF, heart failure with reduced ejection fraction, and donor control subjects. OGDHL expression was quantified in hiPS-CMs treated with or without anti-OPN antibody. Cardiac parameters were evaluated in Col4a3-/- mice with and without global OPN knockout or AAV9-mediated delivery of 2-oxoglutarate dehydrogenase-like (Ogdhl) to the heart.METHODSOGDHL mRNA and protein were quantified in myocardial samples from patients with HFpEF, heart failure with reduced ejection fraction, and donor control subjects. OGDHL expression was quantified in hiPS-CMs treated with or without anti-OPN antibody. Cardiac parameters were evaluated in Col4a3-/- mice with and without global OPN knockout or AAV9-mediated delivery of 2-oxoglutarate dehydrogenase-like (Ogdhl) to the heart.OGDHL mRNA and protein displayed abnormal abundances in cardiac biopsies of HFpEF (n = 17) compared with donor control subjects (n = 12; p < 0.01) or heart failure with reduced ejection fraction patients (n = 12; p < 0.05). Blockade of OPN in hiPS-CMs conferred increased OGDHL expression. Col4a3-/- mice demonstrated cardiomyopathy with similarities to HFpEF, including diastolic dysfunction, cardiac hypertrophy and fibrosis, pulmonary edema, and impaired mitochondrial function. The cardiomyopathy was ameliorated by Opn-/- coincident with improved renal function and increased expression of Ogdhl. Heart-specific overexpression of Ogdhl in Col4a3-/- mice also improved cardiac function and cardiomyocyte energy state.RESULTSOGDHL mRNA and protein displayed abnormal abundances in cardiac biopsies of HFpEF (n = 17) compared with donor control subjects (n = 12; p < 0.01) or heart failure with reduced ejection fraction patients (n = 12; p < 0.05). Blockade of OPN in hiPS-CMs conferred increased OGDHL expression. Col4a3-/- mice demonstrated cardiomyopathy with similarities to HFpEF, including diastolic dysfunction, cardiac hypertrophy and fibrosis, pulmonary edema, and impaired mitochondrial function. The cardiomyopathy was ameliorated by Opn-/- coincident with improved renal function and increased expression of Ogdhl. Heart-specific overexpression of Ogdhl in Col4a3-/- mice also improved cardiac function and cardiomyocyte energy state.Col4a3-/- mice present a model of HFpEF secondary to CKD wherein OPN and OGDHL are intermediates, and possibly therapeutic targets.CONCLUSIONSCol4a3-/- mice present a model of HFpEF secondary to CKD wherein OPN and OGDHL are intermediates, and possibly therapeutic targets. BackgroundPatients with chronic kidney disease (CKD) and coincident heart failure with preserved ejection fraction (HFpEF) may constitute a distinct HFpEF phenotype. Osteopontin (OPN) is a biomarker of HFpEF and predictive of disease outcome. We recently reported that OPN blockade reversed hypertension, mitochondrial dysfunction, and kidney failure in Col4a3−/− mice, a model of human Alport syndrome.ObjectivesThe purpose of this study was to identify potential OPN targets in biopsies of HF patients, healthy control subjects, and human induced pluripotent stem cell–derived cardiomyocytes (hiPS-CMs), and to characterize the cardiac phenotype of Col4a3−/− mice, relate this to HFpEF, and investigate possible causative roles for OPN in driving the cardiomyopathy.MethodsOGDHL mRNA and protein were quantified in myocardial samples from patients with HFpEF, heart failure with reduced ejection fraction, and donor control subjects. OGDHL expression was quantified in hiPS-CMs treated with or without anti-OPN antibody. Cardiac parameters were evaluated in Col4a3−/− mice with and without global OPN knockout or AAV9-mediated delivery of 2-oxoglutarate dehydrogenase-like (Ogdhl) to the heart.ResultsOGDHL mRNA and protein displayed abnormal abundances in cardiac biopsies of HFpEF (n = 17) compared with donor control subjects (n = 12; p < 0.01) or heart failure with reduced ejection fraction patients (n = 12; p < 0.05). Blockade of OPN in hiPS-CMs conferred increased OGDHL expression. Col4a3−/− mice demonstrated cardiomyopathy with similarities to HFpEF, including diastolic dysfunction, cardiac hypertrophy and fibrosis, pulmonary edema, and impaired mitochondrial function. The cardiomyopathy was ameliorated by Opn−/− coincident with improved renal function and increased expression of Ogdhl. Heart-specific overexpression of Ogdhl in Col4a3−/− mice also improved cardiac function and cardiomyocyte energy state.ConclusionsCol4a3−/− mice present a model of HFpEF secondary to CKD wherein OPN and OGDHL are intermediates, and possibly therapeutic targets. AbstractBackgroundPatients with chronic kidney disease (CKD) and coincident heart failure with preserved ejection fraction (HFpEF) may constitute a distinct HFpEF phenotype. Osteopontin (OPN) is a biomarker of HFpEF and predictive of disease outcome. We recently reported that OPN blockade reversed hypertension, mitochondrial dysfunction, and kidney failure in Col4a3−/− mice, a model of human Alport syndrome. ObjectivesThe purpose of this study was to identify potential OPN targets in biopsies of HF patients, healthy control subjects, and human induced pluripotent stem cell–derived cardiomyocytes (hiPS-CMs), and to characterize the cardiac phenotype of Col4a3−/− mice, relate this to HFpEF, and investigate possible causative roles for OPN in driving the cardiomyopathy. MethodsOGDHL mRNA and protein were quantified in myocardial samples from patients with HFpEF, heart failure with reduced ejection fraction, and donor control subjects. OGDHL expression was quantified in hiPS-CMs treated with or without anti-OPN antibody. Cardiac parameters were evaluated in Col4a3−/− mice with and without global OPN knockout or AAV9-mediated delivery of 2-oxoglutarate dehydrogenase-like (Ogdhl) to the heart. ResultsOGDHL mRNA and protein displayed abnormal abundances in cardiac biopsies of HFpEF (n = 17) compared with donor control subjects (n = 12; p < 0.01) or heart failure with reduced ejection fraction patients (n = 12; p < 0.05). Blockade of OPN in hiPS-CMs conferred increased OGDHL expression. Col4a3−/− mice demonstrated cardiomyopathy with similarities to HFpEF, including diastolic dysfunction, cardiac hypertrophy and fibrosis, pulmonary edema, and impaired mitochondrial function. The cardiomyopathy was ameliorated by Opn−/− coincident with improved renal function and increased expression of Ogdhl. Heart-specific overexpression of Ogdhl in Col4a3−/− mice also improved cardiac function and cardiomyocyte energy state. ConclusionsCol4a3−/− mice present a model of HFpEF secondary to CKD wherein OPN and OGDHL are intermediates, and possibly therapeutic targets. |
| Author | Granzier, Henk L. Lambert, Guerline Yousefi, Keyvan Takeuchi, Lauro M. Lee, Dong I. Eisenberg, Trevor Hare, Joshua M. Methawasin, Mei Webster, Keith A. Shehadeh, Lina A. Sukkar, Sarah Hahn, Virginia S. Hatzistergos, Konstantinos E. Irion, Camila I. Kass, David A. Ding, Wen |
| AuthorAffiliation | a Department of Molecular and Cellular Pharmacology, University of Miami Leonard M. Miller School of Medicine, Miami, Florida b Interdisciplinary Stem Cell Institute, University of Miami Leonard M. Miller School of Medicine, Miami, Florida e Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland, USA c Department of Medicine, Division of Cardiology, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, USA g Vascular Biology Institute, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, USA h Peggy and Harold Katz Family Drug Discovery Center, University of Miami Leonard M. Miller School of Medicine, Miami, Florida d Department of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ f Department of Cell Biology, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, USA |
| AuthorAffiliation_xml | – name: c Department of Medicine, Division of Cardiology, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, USA – name: f Department of Cell Biology, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, USA – name: b Interdisciplinary Stem Cell Institute, University of Miami Leonard M. Miller School of Medicine, Miami, Florida – name: a Department of Molecular and Cellular Pharmacology, University of Miami Leonard M. Miller School of Medicine, Miami, Florida – name: g Vascular Biology Institute, University of Miami Leonard M. Miller School of Medicine, Miami, Florida, USA – name: d Department of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ – name: e Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland, USA – name: h Peggy and Harold Katz Family Drug Discovery Center, University of Miami Leonard M. Miller School of Medicine, Miami, Florida |
| Author_xml | – sequence: 1 givenname: Keyvan surname: Yousefi fullname: Yousefi, Keyvan organization: Department of Molecular and Cellular Pharmacology, University of Miami Leonard M. Miller School of Medicine, Miami, Florida – sequence: 2 givenname: Camila I. surname: Irion fullname: Irion, Camila I. organization: Interdisciplinary Stem Cell Institute, University of Miami Leonard M. Miller School of Medicine, Miami, Florida – sequence: 3 givenname: Lauro M. surname: Takeuchi fullname: Takeuchi, Lauro M. organization: Interdisciplinary Stem Cell Institute, University of Miami Leonard M. Miller School of Medicine, Miami, Florida – sequence: 4 givenname: Wen surname: Ding fullname: Ding, Wen organization: Department of Molecular and Cellular Pharmacology, University of Miami Leonard M. Miller School of Medicine, Miami, Florida – sequence: 5 givenname: Guerline surname: Lambert fullname: Lambert, Guerline organization: Interdisciplinary Stem Cell Institute, University of Miami Leonard M. Miller School of Medicine, Miami, Florida – sequence: 6 givenname: Trevor surname: Eisenberg fullname: Eisenberg, Trevor organization: Department of Medicine, Division of Cardiology, University of Miami Leonard M. Miller School of Medicine, Miami, Florida – sequence: 7 givenname: Sarah surname: Sukkar fullname: Sukkar, Sarah organization: Department of Medicine, Division of Cardiology, University of Miami Leonard M. Miller School of Medicine, Miami, Florida – sequence: 8 givenname: Henk L. surname: Granzier fullname: Granzier, Henk L. organization: Department of Cellular and Molecular Medicine, University of Arizona, Tucson, Arizona – sequence: 9 givenname: Mei surname: Methawasin fullname: Methawasin, Mei organization: Department of Cellular and Molecular Medicine, University of Arizona, Tucson, Arizona – sequence: 10 givenname: Dong I. surname: Lee fullname: Lee, Dong I. organization: Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland – sequence: 11 givenname: Virginia S. surname: Hahn fullname: Hahn, Virginia S. organization: Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland – sequence: 12 givenname: David A. surname: Kass fullname: Kass, David A. organization: Division of Cardiology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland – sequence: 13 givenname: Konstantinos E. surname: Hatzistergos fullname: Hatzistergos, Konstantinos E. organization: Interdisciplinary Stem Cell Institute, University of Miami Leonard M. Miller School of Medicine, Miami, Florida – sequence: 14 givenname: Joshua M. surname: Hare fullname: Hare, Joshua M. organization: Interdisciplinary Stem Cell Institute, University of Miami Leonard M. Miller School of Medicine, Miami, Florida – sequence: 15 givenname: Keith A. surname: Webster fullname: Webster, Keith A. organization: Department of Molecular and Cellular Pharmacology, University of Miami Leonard M. Miller School of Medicine, Miami, Florida – sequence: 16 givenname: Lina A. surname: Shehadeh fullname: Shehadeh, Lina A. email: LShehadeh@med.miami.edu organization: Interdisciplinary Stem Cell Institute, University of Miami Leonard M. Miller School of Medicine, Miami, Florida |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31146816$$D View this record in MEDLINE/PubMed |
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| Copyright | 2019 American College of Cardiology Foundation American College of Cardiology Foundation Copyright © 2019 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved. 2019. American College of Cardiology Foundation |
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| Keywords | hiPS-CM hiPSC osteopontin mitochondria Alport syndrome OGDHL CM HFpEF OPN HFrEF IVRT isovolumetric relaxation time cardiac myocyte heart failure with preserved ejection fraction 2-oxoglutarate dehydrogenase-like heart failure with reduced ejection fraction human-induced pluripotent stem cell |
| Language | English |
| License | This article is made available under the Elsevier license. Copyright © 2019 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 ObjectType-Undefined-3 These two authors contributed equally. |
| OpenAccessLink | https://proxy.k.utb.cz/login?url=https://www.ncbi.nlm.nih.gov/pmc/articles/6546303 |
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| PublicationTitle | Journal of the American College of Cardiology |
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| PublicationYear | 2019 |
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| Snippet | Patients with chronic kidney disease (CKD) and coincident heart failure with preserved ejection fraction (HFpEF) may constitute a distinct HFpEF phenotype.... AbstractBackgroundPatients with chronic kidney disease (CKD) and coincident heart failure with preserved ejection fraction (HFpEF) may constitute a distinct... BackgroundPatients with chronic kidney disease (CKD) and coincident heart failure with preserved ejection fraction (HFpEF) may constitute a distinct HFpEF... Abnormal OGDHL expression was observed in cardiac biopsies of HFpEF patients compared to healthy donor or HFrEF groups. OGDHL levels were responsive to OPN... |
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| SubjectTerms | Alport syndrome Animals Autoantigens - genetics Bioenergetics Cardiology Cardiomyocytes Cardiomyopathy Cardiovascular Collagen Type IV - genetics Congestive heart failure Coronary artery disease Cytokines Disease Models, Animal Edema Fibrosis Flow velocity Genetic Therapy Genotype & phenotype Heart failure Heart Failure, Diastolic - etiology Heart Failure, Diastolic - metabolism Heart Failure, Diastolic - pathology Heart Failure, Diastolic - therapy HFpEF Hip hiPS-CM Hypertension Hypertrophy Intermediates Ketoglutarate Dehydrogenase Complex - genetics Ketoglutarate Dehydrogenase Complex - metabolism Ketoglutaric acid Kidney diseases Lung diseases Mice Mice, Knockout Mitochondria Mitochondria - metabolism mRNA Myocardium - metabolism Myocardium - pathology Nephritis, Hereditary - complications OGDHL Osteopontin Osteopontin - genetics Osteopontin - metabolism Oxidative Stress Oxoglutarate dehydrogenase (lipoamide) Patients Phenotypes Pluripotency Pulmonary arteries Renal failure Renal function Stem cells Therapeutic applications Ventricle Ventricular Dysfunction, Left - etiology Ventricular Dysfunction, Left - metabolism |
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| Title | Osteopontin Promotes Left Ventricular Diastolic Dysfunction Through a Mitochondrial Pathway |
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