Signaling Pathways in Cardiac Myocyte Apoptosis

被引:149
|
作者
Xia, Peng [1 ]
Liu, Yuening [1 ]
Cheng, Zhaokang [1 ]
机构
[1] Washington State Univ, Coll Pharm, Dept Pharmaceut Sci, PBS 323,205 E Spokane Falls Blvd,POB 1495, Spokane, WA 99210 USA
关键词
TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; ACTIVATED PROTEIN-KINASE; MYOCARDIAL ISCHEMIA/REPERFUSION INJURY; HYPOXIA-INDUCED APOPTOSIS; STRESS-INDUCED APOPTOSIS; CELL-CYCLE REENTRY; ATTENUATES CARDIOMYOCYTE APOPTOSIS; DOXORUBICIN-INDUCED APOPTOSIS; ENDOPLASMIC-RETICULUM STRESS;
D O I
10.1155/2016/9583268
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Cardiovascular diseases, the number 1 cause of death worldwide, are frequently associated with apoptotic death of cardiac myocytes. Since cardiomyocyte apoptosis is a highly regulated process, pharmacological intervention of apoptosis pathways may represent a promising therapeutic strategy for a number of cardiovascular diseases and disorders including myocardial infarction, ischemia/reperfusion injury, chemotherapy cardiotoxicity, and end- stage heart failure. Despite rapid growth of our knowledge in apoptosis signaling pathways, a clinically applicable treatment targeting this cellular process is currently unavailable. To help identify potential innovative directions for future research, it is necessary to have a full understanding of the apoptotic pathways currently known to be functional in cardiac myocytes. Here, we summarize recent progress in the regulation of cardiomyocyte apoptosis by multiple signalingmolecules and pathways, with a focus on the involvement of these pathways in the pathogenesis of heart disease. In addition, we provide an update regarding bench to bedside translation of this knowledge and discuss unanswered questions that need further investigation.
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页数:22
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