Pro-survival signaling of neuroprotectin D1 (Homo sapiens)

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Uncompensated oxidative stress triggers neuroprotectin D1 to inhibit caspase activity via the intrinsic mitochondrial pathway and via the stimulation of BIRC3 leading to pro-survival stimuli. By inhibiting the formation of the Bax/Bcl-xL complex in the mitochondrial membrane, NPD1 decreases the release of Cytochrome c leading to a lower pro-apoptotic activity. Furthermore, NPD1 inhibits the internalization of death-inducing signaling complex (DISC) which is involved in the initiation of apoptosis, thereby promoting survival of the cell. The neuroprotective effect of NPD1 therefore contributes to the management of diseases like Alzheimer's disease, stroke, age-related macular degeneration, traumatic brain injury, Parkinson's disease and other neurodegenerations.