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Fig. 2 | Military Medical Research

Fig. 2

From: Potential therapy strategy: targeting mitochondrial dysfunction in sepsis

Fig. 2

Mitochondria dysfunction in sepsis. The electron transport chain (ETC) dysfunction results in extreme ROS production within mitochondria, which can lead to oxidative damage to mitochondria membrane, ETC activity and mtDNA. Mitochondrial membrane permeability transition results in release of cytochrome C (cyt C) into the cytosol, leading to apoptosis. Increased membrane permeability also makes the Ca2+ reflux into cytoplasm and a consequent disturbance that might further activate related signaling pathways. Mitochondrial ROS can also transport to cytoplasm and induce oxidative stress, following by oxidative stress signaling pathways activation which modulate various cellular functions. ROS released into extracellular space will further take harm to other cells and organs

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