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机构地区:[1]北京军区总医院医务部,北京100070 [2]西南医院病理研究所,重庆400038
出 处:《标记免疫分析与临床》2013年第5期325-328,335,共5页Labeled Immunoassays and Clinical Medicine
基 金:国家自然科学基金资助项目(No.30670919)
摘 要:细胞核DNA(nuclear DNA,nDNA)损伤后诱导细胞凋亡的信号转导途径已经逐渐清晰,而线粒体DNA(mitochondrial DNA,mtDNA)损伤与细胞凋亡之间的关系尚有待进一步明确。目前已有研究结果表明:mtDNA断裂、缺失或功能缺陷能够显著影响细胞凋亡发生率;线粒体缺失细胞(ρ0细胞)同其亲代细胞相比,对多种凋亡诱导因素的反应存在显著差异;ROS的产生并非mtDNA损伤诱导凋亡的必要条件,mtDNA损伤断裂本身可能启动了凋亡的级联反应。但mtDNA的损伤,在细胞凋亡的信号转导途径具体扮演何种角色,还有待深入研究。The signal pathway of apoptosis induced by nuclear DNA damage is getting explicit gradually. But the relationship between the mitochondrial DNA damage and apoptosis remains unclear. The rate of apoptosis is in- fluenced significantly by the break, depletion and dysfunction of mitochondrial DNA. The reaction of p0 cell to several of apoptotie inducible factors is different from its parental cell lines. The generation of ROS is not the es- sential condition of the mitochondria] DNA damage induced apoptosis and the cascade may be initiated by mito- chondrial DNA damage itself. In a word, further study will be needed to know what role does the mitochondrial DNA damage act in the signal pathway.
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