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Verfasst von:Haustein, Ricarda [VerfasserIn]   i
 Trogisch, Felix [VerfasserIn]   i
 Keles, Merve [VerfasserIn]   i
 Hille, Susanne [VerfasserIn]   i
 Fuhrmann, Manuela [VerfasserIn]   i
 Weinzierl, Nina [VerfasserIn]   i
 Hemanna, Shruthi [VerfasserIn]   i
 Thackeray, James [VerfasserIn]   i
 Dou, Yanliang [VerfasserIn]   i
 Zwadlo, Carolin [VerfasserIn]   i
 Froese, Natali [VerfasserIn]   i
 Cordero, Julio [VerfasserIn]   i
 Bengel, Frank [VerfasserIn]   i
 Müller, Oliver J. [VerfasserIn]   i
 Bauersachs, Johann [VerfasserIn]   i
 Dobreva, Gergana [VerfasserIn]   i
 Heineke, Jörg [VerfasserIn]   i
Titel:C1q and tumor necrosis factor related protein 9 protects from diabetic cardiomyopathy by alleviating cardiac insulin resistance and inflammation
Verf.angabe:Ricarda Haustein, Felix A. Trogisch, Merve Keles, Susanne Hille, Manuela Fuhrmann, Nina Weinzierl, Shruthi Hemanna, James Thackeray, Yanliang Dou, Carolin Zwadlo, Natali Froese, Julio Cordero, Frank Bengel, Oliver J. Müller, Johann Bauersachs, Gergana Dobreva and Joerg Heineke
E-Jahr:2023
Jahr:29 January 2023
Umfang:20 S.
Illustrationen:Illustrationen
Fussnoten:Gesehen am 22.08.2024
Titel Quelle:Enthalten in: Cells
Ort Quelle:Basel : MDPI, 2012
Jahr Quelle:2023
Band/Heft Quelle:12(2023), 3, Artikel-ID 443, Seite 1-20
ISSN Quelle:2073-4409
Abstract:(1) Background: Diabetic cardiomyopathy is a major health problem worldwide. CTRP9, a secreted glycoprotein, is mainly expressed in cardiac endothelial cells and becomes downregulated in mouse models of diabetes mellitus; (2) Methods: In this study, we investigated the impact of CTRP9 on early stages of diabetic cardiomyopathy induced by 12 weeks of high-fat diet; (3) Results: While the lack of CTRP9 in knock-out mice aggravated insulin resistance and triggered diastolic left ventricular dysfunction, AAV9-mediated cardiac CTRP9 overexpression ameliorated cardiomyopathy under these conditions. At this early disease state upon high-fat diet, no fibrosis, no oxidative damage and no lipid deposition were identified in the myocardium of any of the experimental groups. Mechanistically, we found that CTRP9 is required for insulin-dependent signaling, cardiac glucose uptake in vivo and oxidative energy production in cardiomyocytes. Extensive RNA sequencing from myocardial tissue of CTRP9-overexpressing and knock-out as well as respective control mice revealed that CTRP9 acts as an anti-inflammatory mediator in the myocardium. Hence, CTRP9 knock-out exerted more, while CTRP9-overexpressing mice showed less leukocytes accumulation in the heart during high-fat diet; (4) Conclusions: In summary, endothelial-derived CTRP9 plays a prominent paracrine role to protect against diabetic cardiomyopathy and might constitute a therapeutic target.
DOI:doi:10.3390/cells12030443
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

kostenfrei: Volltext: https://doi.org/10.3390/cells12030443
 kostenfrei: Volltext: https://www.mdpi.com/2073-4409/12/3/443
 DOI: https://doi.org/10.3390/cells12030443
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:cardiac endothelial cells
 diastolic dysfunction
 high-fat diet
 paracrine signaling
K10plus-PPN:1899358455
Verknüpfungen:→ Zeitschrift

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