细胞凋亡:它的起源

摘要

细胞凋亡可能是发生在细胞生物中的一种程序性坏死。有机化学事件引起细胞的特征变化(形态)和死亡。这些变化包括气泡、细胞收缩、核碎裂、体物质凝结、体聚合物碎裂和整体RNA衰变。由于caspase介导的细胞死亡，典型的成年人每天会损失500亿到700亿个细胞。

描述

细胞凋亡可能是发生在细胞有机体中的一种程序性坏死。有机化学事件引起细胞的特征变化(形态)和死亡。这些变化包括气泡、细胞收缩、核碎裂、体物质凝结、体聚合物碎裂和整体RNA衰变。由于caspase介导的细胞死亡，典型的成年人每天会损失500亿到700亿个细胞。对于一个年龄在8到14岁之间的人类孩子来说，每天大约有200 - 300亿个细胞死亡。与裂孔病不同的是，裂孔病可能是一种由急性细胞损伤引起的创伤性坏死，而半胱天冬酶介导的细胞死亡可能是一种高度调控的相关控制方法，在生物体的整个生命周期中都有益处。例如，在发育良好的人类胚胎中，手指和脚趾的分离是指间细胞承受caspase介导的细胞死亡的结果。与狮身人体病不同，caspasase介导的细胞死亡产生称为凋亡小体的细胞片段，营养细胞准备在细胞内容物溢出到闭合细胞并对其造成伤害之前将其吞噬和带走。因为caspase介导的细胞死亡一旦开始就无法停止，这是一种高度调控的方法。caspasase介导的细胞死亡通常通过两种途径中的一种启动。 Within the intrinsic pathway the cell kills itself as a result of it senses cell stress, whereas within the accidental pathway the cell kills itself as a result of signals from alternative cells. Weak external signals may activate the intrinsic pathway of caspase-mediated cell death. Each pathway induces necrobiosis by activating caspases, that are proteases, or enzymes that degrade proteins. The 2 pathways each activate leader caspases that then activate public executioner caspases that then kill the cell by degrading proteins indiscriminately. In addition to its importance as a biological development, defective apoptotic processes are concerned in a very big variety of diseases. Excessive caspase-mediated cell death causes atrophy, whereas associate scant quantity leads to uncontrolled cell proliferation, like cancer. Some factors like Fas receptors and caspases promote caspase-mediated cell death, whereas some members of the Bcl-2 family of proteins inhibit caspase-mediated cell death. The initiation of caspase-mediated cell death is tightly regulated by activation mechanisms, as a result of once caspase-mediated cell death has begun; it inevitably results in the death of the cell. The 2 best-understood activation mechanisms are the intrinsic pathway (also referred to as the mitochondrial pathway) and therefore the accidental pathway. The intrinsic pathway is activated by living thing signals generated once cells are stressed and depends on the discharge of proteins from the intermembrane house of mitochondria.The accidental pathway is activated by living thing ligands binding to cell-surface death receptors, that results in the formation of the death-inducing sign complicated (DISC). A cell inductees living thing apoptotic sign in response to a stress, which can bring forth, cell suicide. The required of nuclear receptors by glucocorticoids, heat, radiation, nutrient deprivation, virus infection, hypoxia, inflated living thing concentration of free fatty acids and inflated living thing CA concentration, for instance, by harm to the membrane, will all trigger the discharge of living thing apoptotic signals by a broken cell. Variety of cellular parts, like poly ADP saccharide enzyme, may facilitate regulate caspase-mediated cell death. Single cell fluctuations are discovered in experimental studies of stress elicited caspase-mediated cell death.