Protease-activated receptor 4 deficiency offers cardioprotection after acute ischemia reperfusion injury
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- 作者：Mikhail A. Kolpakova ; Khadija Rafiqb ; Xinji Guoa ; Bahman Hooshdarana ; Tao Wanga ; Liudmila Vlasenkoa ; c ; Yulia V. Bashkirovaa ; Xiaoxiao Zhanga ; Xiongwen Chena ; Sahar Iftikhara ; Joseph R. Libonatid ; Satya P. Kunapulia ; Abdelkarim Sabria ; sabri@temple.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：AAR ; area at risk ; AP ; agonist peptide ; Cat.G ; cathepsin G ; cTnI ; cardiac troponin I ; EGFR ; epidermal growth factor receptor ; IA ; infarct area ; IR ; ischemia&ndash ; reperfusion ; KO ; knockout ; LAD ; left anterior descending ; LV ; left ventricular ; MPO ; myeloperoxidase ; NRCMs ; neonatal rat cardiac myocytes ; PAR ; protease-activated receptor ; TTC ; triphenyltretrazolium chloride ; TUNEL ; terminal deoxynucleotidyl transferase dUTP nick end labeling ; WT ; wild-type
- 刊名：Journal of Molecular and Cellular Cardiology
- 出版年：2016
- 出版时间：January 2016
- 年：2016
- 卷：90
- 期：Complete
- 页码：21-29
- 全文大小：1688 K
文摘
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PAR4 deficiency is cardioprotective after acute myocardial ischemia reperfusion injury.
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PAR4 deletion reduces inflammation after acute ischemia reperfusion injury.
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PAR4 mediates thrombin-induced myocyte apoptosis in vitro.
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PAR4 induces myocyte apoptosis through activation of the JNK pathway.