【摘要】：線粒體通透轉(zhuǎn)換特性自20世紀(jì)70年代被發(fā)現(xiàn)以來,在調(diào)控細(xì)胞凋亡作用方面已獲得廣泛認(rèn)可。該特性由線粒體通透性轉(zhuǎn)換孔(mPTP)介導(dǎo),以線粒體內(nèi)膜通透性升高,相對分子質(zhì)量1.5×10~3的小分子物質(zhì)自由通過線粒體膜為特征,但該通道的分子結(jié)構(gòu)仍不十分清楚。探究mPTP的具體組成與調(diào)節(jié)機(jī)制,有助于提高對神經(jīng)退行性疾病、心血管疾病及癌癥發(fā)病機(jī)制與治療手段的認(rèn)識。本文通過對mPTP結(jié)構(gòu)模型及其調(diào)控細(xì)胞程序性死亡(PCD)具體分子機(jī)制新進(jìn)展的簡要綜述,論證了將mPTP靶向化合物作為PCD調(diào)控藥物的可行性。
[Abstract]:Since the discovery of mitochondrial permeability conversion in the 1970s, it has been widely recognized in the regulation of apoptosis. This characteristic was mediated by mitochondrial permeability transition pore (mPTP), which was characterized by the increase of mitochondrial intimal permeability and the free passage of small molecular matter with relative molecular weight of 1.5 脳 10 ~ (-3) through the mitochondrial membrane, but the molecular structure of the channel was not very clear. It is helpful to understand the pathogenesis and treatment of neurodegenerative diseases, cardiovascular diseases and cancer by exploring the specific components and regulatory mechanisms of mPTP. In this paper, a brief review of the mPTP structural model and the new progress in the molecular mechanism of (PCD) regulating cell programmed death is presented, and the feasibility of using mPTP targeting compounds as PCD regulatory drugs is demonstrated.
【作者單位】： 江蘇大學(xué)藥學(xué)院 線粒體與神經(jīng)生物學(xué)試驗(yàn)室;
【基金】：國家自然科學(xué)基金資助項(xiàng)目(81503051) 江蘇省自然科學(xué)基金資助項(xiàng)目(BK20140574) 江蘇大學(xué)高級專業(yè)人才科研啟動(dòng)基金項(xiàng)目(13JDG063);江蘇大學(xué)青年骨干教師培育計(jì)劃
【分類號】：R91

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