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Table 4 Autophagy in acute neuronal injury.

From: All-you-can-eat: autophagy in neurodegeneration and neuroprotection

Injury Autophagy related changes Ref.
Hypoxia/Ischemia Mixed results after hypoxic treatments: Knockout of Atg genes in C. elegans decreases survival after hypoxia and autophagy activation by rapamycin treatment leads to injury reduction in rat and rat tissue. On the contrary, Atg7-/- mice lacking functional autophagy in the CNS are largely protected from neurodegeneration. [247, 80, 104, 94, 244, 246, 245]
Trauma Macroautophagy appears to be beneficial: Autophagy can be activated for more than a month following brain trauma (elevated BECN1, MAP1LC3-II, ATG5-12 levels, increased AV numbers) in rodents, autophagy appears activated in human tissue samples. Rapamycin treatment is neuroprotective in mice. [106, 87, 249, 248, 65, 95, 84, 81, 250]
Pharmacological injury Autophagy appears to be deleterious: Transient activation of autophagy after injury (elevated MAP1LC3-II, p-mTOR, LAMP2, increased AV numbers) and activation of apoptosis in rodents and primary neuronal culture. 3-MA treatment or RNAi against ATG5 or BECN1 blocks cell death. [96, 252, 166, 103, 253, 251, 254]
Trophic deprivation Autophagy appears to be deleterious: Growth factor withdrawal leads to autophagic cell death in rodents or chicken, 3-MA blocks cytochrome C release and delays apoptosis. [257, 255, 256, 259, 258]