PTEN induced putative kinase 1 (PINK1) alleviates angiotensin II-induced cardiac injury by ameliorating mitochondrial dysfunction

Xiong, Wenjun; Hua, Jinghai; Liu, Zuheng; Cai, Wanqiang; Bai, Yujia; Zhan, Qiong; Lai, Wenyan; Zeng, Qingchun; Ren, Hao; Xu, Dingli

doi:10.1016/j.ijcard.2018.03.054

Title: PTEN induced putative kinase 1 (PINK1) alleviates angiotensin II-induced cardiac injury by ameliorating mitochondrial dysfunction

Full Record
Other Related Research

Authors:: Xiong, Wenjun; Hua, Jinghai; Liu, Zuheng; Cai, Wanqiang; Bai, Yujia; Zhan, Qiong; Lai, Wenyan; Zeng, Qingchun; Ren, Hao; Xu, Dingli

Publication Date:: Sat Sep 01 00:00:00 EDT 2018

Sponsoring Org.:: USDOE Office of Electricity (OE), Advanced Grid Research & Development. Power Systems Engineering Research

OSTI Identifier:: 1693711

Grant/Contract Number:: 2017YFC 1308304

Resource Type:: Publisher's Accepted Manuscript

Journal Name:: International Journal of Cardiology

Additional Journal Information:: Journal Name: International Journal of Cardiology Journal Volume: 266 Journal Issue: C; Journal ID: ISSN 0167-5273

Publisher:: Elsevier

Country of Publication:: Netherlands

Language:: English

Citation Formats


                    Xiong, Wenjun, Hua, Jinghai, Liu, Zuheng, Cai, Wanqiang, Bai, Yujia, Zhan, Qiong, Lai, Wenyan, Zeng, Qingchun, Ren, Hao, and Xu, Dingli. PTEN induced putative kinase 1 (PINK1) alleviates angiotensin II-induced cardiac injury by ameliorating mitochondrial dysfunction.  Netherlands: N. p., 2018. 
Web.  doi:10.1016/j.ijcard.2018.03.054.

Copy to clipboard


                    Xiong, Wenjun, Hua, Jinghai, Liu, Zuheng, Cai, Wanqiang, Bai, Yujia, Zhan, Qiong, Lai, Wenyan, Zeng, Qingchun, Ren, Hao, & Xu, Dingli. PTEN induced putative kinase 1 (PINK1) alleviates angiotensin II-induced cardiac injury by ameliorating mitochondrial dysfunction.  Netherlands.  https://doi.org/10.1016/j.ijcard.2018.03.054

Copy to clipboard


                    Xiong, Wenjun, Hua, Jinghai, Liu, Zuheng, Cai, Wanqiang, Bai, Yujia, Zhan, Qiong, Lai, Wenyan, Zeng, Qingchun, Ren, Hao, and Xu, Dingli. Sat .  
"PTEN induced putative kinase 1 (PINK1) alleviates angiotensin II-induced cardiac injury by ameliorating mitochondrial dysfunction".  Netherlands.  https://doi.org/10.1016/j.ijcard.2018.03.054.

Copy to clipboard


                    
@article{osti_1693711,

  title        = {PTEN induced putative kinase 1 (PINK1) alleviates angiotensin II-induced cardiac injury by ameliorating mitochondrial dysfunction},

  author       = {Xiong, Wenjun and Hua, Jinghai and Liu, Zuheng and Cai, Wanqiang and Bai, Yujia and Zhan, Qiong and Lai, Wenyan and Zeng, Qingchun and Ren, Hao and Xu, Dingli},

  abstractNote = {},

  doi          = {10.1016/j.ijcard.2018.03.054},

  journal      = {International Journal of Cardiology},

  number       = C,

  volume       = 266,

  place        = {Netherlands},

  year         = {Sat Sep 01 00:00:00 EDT 2018},

  month        = {Sat Sep 01 00:00:00 EDT 2018}

}

Copy to clipboard

Journal Article:

Free Publicly Available Full Text

Accepted Manuscript (Publisher)

Publisher's Version of Record
https://doi.org/10.1016/j.ijcard.2018.03.054

Other availability

Search WorldCat to find libraries that may hold this journal

Save / Share:

Export Metadata

Save to My Library

Similar Records in DOE PAGES and OSTI.GOV collections:

PINK1 alleviates myocardial hypoxia-reoxygenation injury by ameliorating mitochondrial dysfunction

Journal Article Li, Yang ; Qiu, Liangxian ; Liu, Xiping ; ... - Biochemical and Biophysical Research Communications

PTEN inducible kinase-1 (PINK1) mutant induces mitochondrial dysfunction of cells, resulting in an inherited form of Parkinson's disease. However its exact role in the cardiomyocytes is unclear. The present study examined the function of PINK1 in hypoxia-reoxygenation (H/R) induced H9c2 cell damage and its potential mechanism. The H/R model in H9c2 cells was established by 6 h of hypoxia and 12 h of reoxygenation. The CCK8 and LDH assay indicated that the cell viability was obviously reduced after H/R. The expression of PINK1 was decreased in H/R-induced H9c2 cells compared with control group. The vector overexpressing PINK1 was constructed to transfect intomore »« less
https://doi.org/10.1016/J.BBRC.2017.01.061
Inhibition of glycogen synthase kinase 3beta ameliorates triptolide-induced acute cardiac injury by desensitizing mitochondrial permeability transition

Journal Article Wang, Wenwen ; Yang, Yanqin ; Xiong, Zhewen ; ... - Toxicology and Applied Pharmacology

Triptolide (TP), a diterpene triepoxide, is a major active component of Tripterygium wilfordii extracts, which are prepared as tablets and has been used clinically for the treatment of inflammation and autoimmune disorders. However, TP's therapeutic potential is limited by severe adverse effects. In a previous study, we reported that TP induced mitochondria dependent apoptosis in cardiomyocytes. Glycogen synthase kinase-3β (GSK-3β) is a multifunctional serine/threonine kinase that plays important roles in the necrosis and apoptosis of cardiomyocytes. Our study aimed to investigate the role of GSK-3β in TP-induced cardiotoxicity. Inhibition of GSK-3β activity by SB 216763, a potent and selective GSK-3more »« less
https://doi.org/10.1016/J.TAAP.2016.10.007
Alleviation of CCCP-induced mitochondrial injury by augmenter of liver regeneration via the PINK1/Parkin pathway-dependent mitophagy

Journal Article Zhang, Jing ; Chen, Sili ; Li, Ye ; ... - Experimental Cell Research

The occurrence of liver diseases is attributed to mitochondrial damage. Mitophagy selectively removes dysfunctional mitochondria, thereby preserving mitochondrial function. Augmenter of liver regeneration (ALR) protects the mitochondria from injury. However, whether ALR protection is associated with mitophagy remains unclear. In this study, mitochondrial damage was induced by carbonyl cyanide 3-chlorophenylhydrazone (CCCP), and long-form ALR (lfRNA)-mediated protection against this damage was investigated. Treatment of HepG2 cells with CCCP elevated the level of intracellular ROS, inhibited ATP production, and increased the mitochondrial membrane potential and cell apoptotic rate. However, in lfALR-transfected cells, CCCP-induced cell injury was clearly alleviated, the apoptosis and ROSmore »« less
https://doi.org/10.1016/J.YEXCR.2021.112866
Roles of PTEN-induced putative kinase 1 and dynamin-related protein 1 in transient global ischemia-induced hippocampal neuronal injury

Journal Article Chen, Shang-Der ; Center for Translational Research in Biomedical Sciences, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taiwan ; Lin, Tsu-Kung ; ... - Biochemical and Biophysical Research Communications

Recent studies showed that increased mitochondrial fission is an early event of cell death during cerebral ischemia and dynamin-related protein 1 (Drp1) plays an important role in mitochondrial fission, which may be regulated by PTEN-induced putative kinase 1 (PINK1), a mitochondrial serine/threonine-protein kinase thought to protect cells from stress-induced mitochondrial dysfunction and regulate mitochondrial fission. However, the roles of PINK1 and Drp1 in hippocampal injury caused by transient global ischemia (TGI) remain unknown. We therefore tested the hypothesis that TGI may induce PINK1 causing downregulation of Drp1 phosphorylation to enhance hippocampal neuronal survival, thus functioning as an endogenous neuroprotective mechanism.more »« less
https://doi.org/10.1016/J.BBRC.2015.03.045
Adipokine CTRP6 improves PPARγ activation to alleviate angiotensin II-induced hypertension and vascular endothelial dysfunction in spontaneously hypertensive rats

Journal Article Chi, Liyi ; Departments of Cardiology, The 451st Hospital of People's Liberation Army ; Hu, Xiaojing ; ... - Biochemical and Biophysical Research Communications

Angiotensin II (AngII) is the most important component of angiotensin, which has been regarded as a major contributor to the incidence of hypertension and vascular endothelial dysfunction. The adipocytokine C1q/TNF-related protein 6 (CTRP6) was recently reported to have multiple protective effects on cardiac and cardiovascular function. However, the exact role of CTRP6 in the progression of AngII induced hypertension and vascular endothelial function remains unclear. Here, we showed that serum CTRP6 content was significantly downregulated in SHRs, accompanied by a marked increase in arterial systolic pressure and serum AngII, CRP and ET-1 content. Then, pcDNA3.1-mediated CTRP6 delivery or CTRP6 siRNAmore »« less
https://doi.org/10.1016/J.BBRC.2016.11.102

Similar Records