Mitochondria and apoptosis regulation
Zhu Yu-shan
Abstract
Zhu Yu-shan
Abstract
Apoptosis is a highly regulated form of programmed cell death,which plays a key role in the development and homeostasis of multicellular organisms.Mitochondria play a central role in the regulation of apoptotic cell death.Upon death stimuli,different apoptogenic factors such as cytochrome c and Smac/Diablo are released during the early stages of apoptosis.A small amount cytochrome c may be sufficient for activating caspases.Once activated,caspases can positively feedback to attack mitochondria leading to a more profound loss of cytochrome c and consequently mitochondrial dysfunction.This caspase-mediated late stage of cyto- chrome c release causes the complete disruption of mitochondrial electron transport chain,leading to the increase in cellular ROS and complete loss of ATP generation,late stage of apoptotic events or secondary necrosis.Bcl-2 and its family proteins are important for regulating cytochrome c release and apoptotic processes.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Apoptosis is a highly regulated form of programmed cell death,which plays a key role in the development and homeostasis of multicellular organisms.Mitochondria play a central role in the regulation of apoptotic cell death.Upon death stimuli,different apoptogenic factors such as cytochrome c and Smac/Diablo are released during the early stages of apoptosis.A small amount cytochrome c may be sufficient for activating caspases.Once activated,caspases can positively feedback to attack mitochondria leading to a more profound loss of cytochrome c and consequently mitochondrial dysfunction.This caspase-mediated late stage of cyto- chrome c release causes the complete disruption of mitochondrial electron transport chain,leading to the increase in cellular ROS and complete loss of ATP generation,late stage of apoptotic events or secondary necrosis.Bcl-2 and its family proteins are important for regulating cytochrome c release and apoptotic processes.
Key concepts: Cytochrome c, Apoptosis, Cell biology, Mitochondrion, Apoptosome, Caspase, Programmed cell death, Biology