作者: Tomoka Takatani-Nakase , Koichi Takahashi
DOI: 10.1016/J.BBRC.2015.05.008
关键词: Internal medicine 、 Pi 、 Biology 、 Myocyte 、 Programmed cell death 、 Mechanism (biology) 、 Apoptotic cell death 、 Ischemia 、 Hormone 、 Leptin 、 Endocrinology
摘要: Caspase-independent, non-apoptotic cell death is an important therapeutic target in myocardial ischemia. Leptin, adipose-derived hormone, known to exhibit cytoprotective effects on the ischemic heart, but mechanisms are poorly understood. In this research, we found that pretreatment of leptin strongly suppressed ischemic-augmented nuclear shrinkage and cardiomyocytes. Leptin was also shown significantly inhibit activity iPLA2, which considered play crucial roles death, resulting effective prevention ischemia-induced myocyte death. These findings provide first evidence a protective mechanism against cardiomyocyte