The role of autophagy in the regulation of neuroinflammation in acute ischemic stroke (review of literature).
A V LugovayaT S EmanuelN M KalininaV Ph MitreikinA V ArtemovaA A MakienkoPublished in: Klinicheskaia laboratornaia diagnostika (2022)
Postischemic neuroinflammation is a critical pathophysiological process within the entire scheme of cerebral ischemia, covering early damage and the period of tissue repair. It is characterized by microglial and astroglial activation with increased expression of inflammatory mediators and is accompanied by impaired innate and adaptive immune responses. In acute ischemic stroke (IS), neuroinflammation is caused by the response of resident immune cells of microglia and peripheral immunocompetent cells infiltrating the brain tissue, which penetrate the blood-brain barrier (BBB) into the lesion. Recent studies have shown the important role of the NLRP3-mediated inflammation in the death of neurons and glial cells in acute IS. The review presents the main mechanisms of activation of NLRP3-mediated inflammation in acute IS, leading to the caspase-1 formation and the IL-1β and IL-18 release, which are involved in the initiation and progression of inflammation in the brain parenchyma. The literature data on the role of autophagy in the inhibition of postischemic neuroinflammation are summarized. Autophagy can suppress neuroinflammation through a wide range of the autophagy - related proteins. The role of autophagy as a negative regulator of NLRP3-mediated inflammation in acute IS is analyzed. Data on the participation of autophagic proteins Beclin-1, LC3, and p62 in the suppression of NLRP3 inflammation due to the induction of basic mitophagy are presented. Prospects for modulating autophagy aimed at suppressing postischemic neuroinflammation, including the inhibition of NLRP3-inflammasome, have been noted. The review was based on sources from international and national data bases: Scopus, Web of Science, Springer, RINC.
Keyphrases
- physical activity
- oxidative stress
- cerebral ischemia
- induced apoptosis
- cell death
- nlrp inflammasome
- endoplasmic reticulum stress
- signaling pathway
- lipopolysaccharide induced
- blood brain barrier
- subarachnoid hemorrhage
- cell cycle arrest
- lps induced
- traumatic brain injury
- immune response
- brain injury
- liver failure
- inflammatory response
- cognitive impairment
- respiratory failure
- electronic health record
- big data
- spinal cord
- hepatitis b virus
- machine learning
- white matter
- mass spectrometry
- simultaneous determination
- spinal cord injury
- aortic dissection
- toll like receptor
- binding protein
- patient safety
- pi k akt
- dendritic cells
- extracorporeal membrane oxygenation