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Tumor Necrosis Factor Receptor-Associated Protein 1 Protects against Mitochondrial Injury by Preventing High Glucose-Induced mPTP Opening in Diabetes
Joint Authors
Liu, Lerong
Zhang, Lingxiao
Zhao, Jiangpei
Guo, Xiangyu
Luo, Yuanyuan
Hu, Wenli
Zhao, Tongfeng
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2020, Issue 2020 (31 Dec. 2020), pp.1-17, 17 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2020-03-06
Country of Publication
Egypt
No. of Pages
17
Main Subjects
Abstract EN
Diabetic kidney disease (DKD) has become the leading cause of end-stage renal disease worldwide.
Renal tubular epithelial cell apoptosis and tubular atrophy have been recognized as indicators of the severity and progression of DKD, while the mechanism remains elusive.
Tumor necrosis factor receptor-associated protein 1 (TRAP1) plays critical roles in apoptosis.
The aim of this study was to investigate the protective role TRAP1 plays in DKD and to study the potential underlying mechanisms.
TRAP1 expression was decreased, and mitochondria were injured in NRK-52e cells under high-glucose (HG) conditions.
The overexpression of TRAP1 ameliorated HG-induced apoptosis, increased cell viability, maintained mitochondrial morphology, adenosine triphosphate (ATP) levels, and mitochondrial membrane potential (MMP), and buffered oxidative stress, whereas TRAP1 knockdown aggravated these effects.
The protective effects of TRAP1 may be exerted via the inhibition of mitochondrial permeability transition pore (mPTP) opening, and the damage caused by TRAP1 knockdown can be partially reversed by treatment with the mPTP opening inhibitor cyclosporin A (CsA).
In vivo, TRAP1 expression upregulation by AAV2/9 injection prevented renal dysfunction, ameliorated histopathological changes, maintained mitochondrial morphology and function, and reduced apoptosis and reactive oxygen species (ROS) in STZ-treated DKD rats.
Thus, our results suggest that TRAP1 ameliorates diabetes-induced renal injury by preventing abnormal mPTP opening and maintaining mitochondrial structure and function, which may be treated as a potential target for DKD treatment.
American Psychological Association (APA)
Liu, Lerong& Zhang, Lingxiao& Zhao, Jiangpei& Guo, Xiangyu& Luo, Yuanyuan& Hu, Wenli…[et al.]. 2020. Tumor Necrosis Factor Receptor-Associated Protein 1 Protects against Mitochondrial Injury by Preventing High Glucose-Induced mPTP Opening in Diabetes. Oxidative Medicine and Cellular Longevity،Vol. 2020, no. 2020, pp.1-17.
https://search.emarefa.net/detail/BIM-1205132
Modern Language Association (MLA)
Liu, Lerong…[et al.]. Tumor Necrosis Factor Receptor-Associated Protein 1 Protects against Mitochondrial Injury by Preventing High Glucose-Induced mPTP Opening in Diabetes. Oxidative Medicine and Cellular Longevity No. 2020 (2020), pp.1-17.
https://search.emarefa.net/detail/BIM-1205132
American Medical Association (AMA)
Liu, Lerong& Zhang, Lingxiao& Zhao, Jiangpei& Guo, Xiangyu& Luo, Yuanyuan& Hu, Wenli…[et al.]. Tumor Necrosis Factor Receptor-Associated Protein 1 Protects against Mitochondrial Injury by Preventing High Glucose-Induced mPTP Opening in Diabetes. Oxidative Medicine and Cellular Longevity. 2020. Vol. 2020, no. 2020, pp.1-17.
https://search.emarefa.net/detail/BIM-1205132
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1205132