Lemasters J J
Department of Cell Biology & Anatomy, University of North Carolina, Chapel Hill, North Carolina 27799-7090, USA.
Am J Physiol. 1999 Jan;276(1):G1-6. doi: 10.1152/ajpgi.1999.276.1.G1.
Opening of a high-conductance pore conducting solutes of molecular mass <1,500 Da causes onset of the mitochondrial permeability transition (MPT). Cyclosporin A blocks this pore and prevents acute necrotic cell death in several models. Confocal microscopy directly visualizes onset of the MPT during acute cytotoxicity from the movement of the green-fluorescing fluorophore, calcein, into the mitochondria from the cytosol. The MPT also plays a causative role in tumor necrosis factor-alpha-induced apoptosis in hepatocytes. Progression to apoptosis or necrosis after the MPT may depend on the presence or absence, respectively, of ATP. Often, features of both apoptotic and necrotic cell death develop after death signals and toxic stresses. The term "necrapoptosis" is introduced to emphasize the shared pathways leading to both forms of cell death.
分子量小于1500道尔顿的高电导孔传导溶质的开放会引发线粒体通透性转换（MPT）。在多种模型中，环孢素A可阻断此孔并防止急性坏死性细胞死亡。共聚焦显微镜通过绿色荧光团钙黄绿素从细胞质进入线粒体的运动，直接观察到急性细胞毒性过程中MPT的发生。MPT在肿瘤坏死因子-α诱导的肝细胞凋亡中也起因果作用。MPT后凋亡或坏死的进展可能分别取决于ATP的存在与否。通常，凋亡和坏死性细胞死亡的特征在死亡信号和毒性应激后都会出现。引入“坏死性凋亡”一词是为了强调导致这两种细胞死亡形式的共同途径。
