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TANK-binding kinase 1 alleviates myocardial ischemia/reperfusion injury through regulating apoptotic pathway.
Metadata
Journalbiochemical and biophysical research communications2.985Date
2020 Jun 03
4 months ago
Type
Journal Article
Volume
2020-Jul-30 / 528 : 574-579
Author
Lv P 1, Li C 2, Wang M 3, Ren J 4, Zhang Y 5, Fu G 6
Affiliation
  • 2. Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
  • 3. Department of Cardiology, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, 310020, Hangzhou, Zhejiang, China; Key Laboratory of Cardiovascular Intervention and Regenerative Medicine of Zhejiang Province, Hangzhou, Zhejiang, China.
  • 4. Department of Cardiology, Zhongshan Hospital, Fudan University, 200032, Shanghai, China; Shanghai Institute of Cardiovascular Diseases, Shanghai, China; Center for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY, 82071, USA.
  • 5. Department of Cardiology, Zhongshan Hospital, Fudan University, 200032, Shanghai, China; Shanghai Institute of Cardiovascular Diseases, Shanghai, China. Electronic address: [email protected]
  • 6. Department of Cardiology, Sir Run Run Shaw Hospital, Medical School of Zhejiang University, 310020, Hangzhou, Zhejiang, China; Key Laboratory of Cardiovascular Intervention and Regenerative Medicine of Zhejiang Province, Hangzhou, Zhejiang, China. Electronic address: [email protected]
Doi
PMIDMESH
Abstract
Myocardial ischemia/reperfusion (MI/R) injury, a complicated pathophysiological process, is regulated by lots of signaling pathways. Here in our present study, we identified TANK-binding kinase 1 (TBK1), an IKK-related serine/threonine kinase, as a protective regulator in MI/R injury. Our results indicated that TBK1 was decreased in MI/R injury in mice. However, after overexpressing TBK1 through an intramyocardial injection of TBK1 adenovirus, TBK1 overexpression improved cardiac function detected by echocardiography, decreased infarct size detected by Evans Blue and TTC staining, reduced cardiomyocyte apoptosis measured by TUNEL staining and alleviated disruption of mitochondria and cardiac muscle fibers detected by TEM in response to MI/R injury. Consistently, TBK1 overexpression ameliorated mitochondrial oxygen consumption rate (OCR) in neonatal rat cardiomyocytes (NRCMs) in response to hypoxia/reoxygenation (H/R) injury. Mechanistically, TBK1 overexpression upregulated Bcl-2 (an anti-apoptotic protein) but downregulated Bax (a pro-apoptotic protein) in vivo and in vitro. Collectively, our findings uncovered a pivotal function of TBK1 in MI/R injury through regulating the levels of apoptotic proteins for the first time, which might represent a promising target in treating MI/R patients in the future.
Keywords: Apoptotic proteins Myocardial ischemia/reperfusion OCR TANK-Binding kinase 1 TBK1 adenovirus
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Biochem Biophys Res Communbiochemical and biophysical research communications
Metadata
LocationUnited States
FromACADEMIC PRESS INC ELSEVIER SCIENCE

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