| Literature DB >> 27256553 |
Lorenzo Galluzzi1,2,3,4,5, José Manuel Bravo-San Pedro1,2,3,4,5, Klas Blomgren6, Guido Kroemer1,2,3,4,6,7,8.
Abstract
Autophagy is an evolutionarily ancient mechanism that ensures the lysosomal degradation of old, supernumerary or ectopic cytoplasmic entities. Most eukaryotic cells, including neurons, rely on proficient autophagic responses for the maintenance of homeostasis in response to stress. Accordingly, autophagy mediates neuroprotective effects following some forms of acute brain damage, including methamphetamine intoxication, spinal cord injury and subarachnoid haemorrhage. In some other circumstances, however, the autophagic machinery precipitates a peculiar form of cell death (known as autosis) that contributes to the aetiology of other types of acute brain damage, such as neonatal asphyxia. Here, we dissect the context-specific impact of autophagy on non-infectious acute brain injury, emphasizing the possible therapeutic application of pharmacological activators and inhibitors of this catabolic process for neuroprotection.Entities:
Mesh:
Substances:
Year: 2016 PMID: 27256553 DOI: 10.1038/nrn.2016.51
Source DB: PubMed Journal: Nat Rev Neurosci ISSN: 1471-003X Impact factor: 34.870