热休克蛋白60(heat shock protein 60,HSP60)是主要存在于线粒体内的分子伴侣蛋白,对于维持线粒体蛋白的正常结构和功能不可或缺。线粒体中的HSP60可作用于凋亡相关因子而抑制线粒体凋亡通路的激活,并且能够减少线粒体产生氧自由基;胞...热休克蛋白60(heat shock protein 60,HSP60)是主要存在于线粒体内的分子伴侣蛋白,对于维持线粒体蛋白的正常结构和功能不可或缺。线粒体中的HSP60可作用于凋亡相关因子而抑制线粒体凋亡通路的激活,并且能够减少线粒体产生氧自由基;胞浆中的少量HSP60亦可通过与凋亡相关因子的相互作用等途径抑制细胞凋亡。相反,在某些刺激因素作用下或者HSP60细胞定位异常时,HSP60可产生促凋亡效应。HSP60在细胞凋亡中的双重作用及其对于肿瘤等疾病诊治的意义已引起高度关注。展开更多
Endothelin (ET) is a family of potent vasoconstrictive peptides mainly distributed in the cardiovascular system. ET 1, the primary isoform of ET in the cardiovascular system, is produced by endothelial cells, cardiomy...Endothelin (ET) is a family of potent vasoconstrictive peptides mainly distributed in the cardiovascular system. ET 1, the primary isoform of ET in the cardiovascular system, is produced by endothelial cells, cardiomyocytes and smooth muscle cells. Exogenous ET 1 was shown to not only result in myocardial ischemia and arrhythmia via coronary constriction, but also to have pro ischemic and pro arrhythmogenic effects. Endogenous ET 1 is involved in myocardial ischemia/hypoxia. It has been reported that short time ischemia no longer than several minutes could cause release of ET 1 from ischemic myocardium, and longer time ischemia up regulation of ET 1 biosynthesis in ischemic myocardium. Similar to the effects of exogenous ET 1, increased endogenous ET 1 during ischemia tend to aggravate myocardial ischemia via coronary constriction, and exert pro ischemic and pro arrhythmogenic effects as well. It possibly contributes to the genesis of ischemic arrhythmia. This article chiefly reviewed the studies on exogenous ET 1 and arrhythmia, and endogenous ET 1 in ischemic arrhythmia.展开更多
随着对甾体激素作用机理研究的深入发展,越来越多的实验结果表明,甾体激素不仅能通过与细胞内的受体结合,进而影响 DNA 转录而发挥甾体激素重要的调节功能,它还能与位于细胞膜上的特导结合位点(膜受体?)结合,产生某些潜伏期极短的快效...随着对甾体激素作用机理研究的深入发展,越来越多的实验结果表明,甾体激素不仅能通过与细胞内的受体结合,进而影响 DNA 转录而发挥甾体激素重要的调节功能,它还能与位于细胞膜上的特导结合位点(膜受体?)结合,产生某些潜伏期极短的快效应。迄今为止,已有少量文献报道在大鼠脑。展开更多
文摘热休克蛋白60(heat shock protein 60,HSP60)是主要存在于线粒体内的分子伴侣蛋白,对于维持线粒体蛋白的正常结构和功能不可或缺。线粒体中的HSP60可作用于凋亡相关因子而抑制线粒体凋亡通路的激活,并且能够减少线粒体产生氧自由基;胞浆中的少量HSP60亦可通过与凋亡相关因子的相互作用等途径抑制细胞凋亡。相反,在某些刺激因素作用下或者HSP60细胞定位异常时,HSP60可产生促凋亡效应。HSP60在细胞凋亡中的双重作用及其对于肿瘤等疾病诊治的意义已引起高度关注。
文摘Endothelin (ET) is a family of potent vasoconstrictive peptides mainly distributed in the cardiovascular system. ET 1, the primary isoform of ET in the cardiovascular system, is produced by endothelial cells, cardiomyocytes and smooth muscle cells. Exogenous ET 1 was shown to not only result in myocardial ischemia and arrhythmia via coronary constriction, but also to have pro ischemic and pro arrhythmogenic effects. Endogenous ET 1 is involved in myocardial ischemia/hypoxia. It has been reported that short time ischemia no longer than several minutes could cause release of ET 1 from ischemic myocardium, and longer time ischemia up regulation of ET 1 biosynthesis in ischemic myocardium. Similar to the effects of exogenous ET 1, increased endogenous ET 1 during ischemia tend to aggravate myocardial ischemia via coronary constriction, and exert pro ischemic and pro arrhythmogenic effects as well. It possibly contributes to the genesis of ischemic arrhythmia. This article chiefly reviewed the studies on exogenous ET 1 and arrhythmia, and endogenous ET 1 in ischemic arrhythmia.
