Figure 2.

Plausible mechanism of inhibition of autophagy flux in secondary injury process during acute phase of moderate traumatic SCI and the outcomes.

Several factors such as excessive generation of ROS due to mitochondrial dysfunction, cleavage of HSP70 by calpain activity, and channel-forming Bax are likely to contribute to the damage in lysosomal membrane leading to lysosomal dysfunction and ER stress may cause destabilization of autophagosomal membrane leading to failure in formation of functional autolysosome and thus inhibition of autophagy flux. Inhibition of autophagy flux promotes excessive apoptosis in neurons and oligodendrocytes resulting in neurological dysfunctions. ER: Endoplasmic reticulum; HSP70: heat shock protein 70; ROS: reactive oxygen species; SCI: spinal cord injury.