内质网应激与心血管疾病

的激活使内质网应激能够独立地诱导凋亡,而不依赖于其它通路。这说明在不同的心力衰竭模型中,JNK、caspase-12和CHOP三条途径可能在ERS 反应性凋亡中占有不同的地位,甚至ERS反应性凋亡本身所起作用大小也不一样。Р参考文献:Р[1]刘秀华. 缺血后处理内源性心脏保护的研究进展[J]. 生理学报,2007,59(5):628-634.Р[2]Bruyninx M,Hennuy B, A,et al. A novel gene overexpressedin the prostate of castrated rats:hormonal regulation,relationshipto apoptosis and to acquired prostatic cell androgen independence[J]. Endocrinology,1999,140(10):4789-4799.Р[3]Isodono K,Takahashi T,Imoto H,et al. PARM-1 is an endoplasmicreticulum molecule involved in endoplasmic reticulumstress-induced apoptosis in rat cardiac myocytes[J]. PLoS One,2010,5(3):e974601-e974610.Р[4]Matsushita E,Asai N,Enomoto A,et al. Protective role of gipie,a girdin family proteinР,in endoplasmic reticulum stress responses inendothelial cells[J]. Mol Biol Cell,2011,22(6):736-747.