Focus on the role of mitochondria in NLRP3 inflammasome activation: A prospective target for the treatment of ischemic stroke (Review)

Post-ischemic neuroinflammation induced by the innate local immune response is a major pathophysiological feature of cerebral ischemic stroke, which remains the leading cause of mortality and disability worldwide. NLR family pyrin domain containing (NLRP)3 inflammasome crucially mediates post-ischem...

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Bibliographic Details
Published in:International journal of molecular medicine 2022-06, Vol.49 (6), p.1, Article 74
Main Authors: Zhang, Xiaolu, Zeng, Wenyun, Zhang, Yue, Yu, Qun, Zeng, Miao, Gan, Jiali, Zhang, Wenlan, Jiang, Xijuan, Li, Huhu
Format: Article
Language:English
Subjects:
Apoptosis
Brain damage
Drug therapy
Glucose
Health aspects
Hypoxia
Immune response
Interleukins
Ischemia
Medical prognosis
Medical research
Medicine, Experimental
Mitochondria
Mitochondrial DNA
Mutation
Nervous system
Neurons
Phosphorylation
Proteins
Stroke
Stroke (Disease)
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Summary:Post-ischemic neuroinflammation induced by the innate local immune response is a major pathophysiological feature of cerebral ischemic stroke, which remains the leading cause of mortality and disability worldwide. NLR family pyrin domain containing (NLRP)3 inflammasome crucially mediates post-ischemic inflammatory responses via its priming, activation and interleukin-1[beta] release during hypoxic-ischemic brain damage. Mitochondrial dysfunctions are among the main hallmarks of several brain diseases, including ischemic stroke. In the present review, focus was addressed on the role of mitochondria in cerebral ischemic stroke while keeping NLRP3 inflammasome as a link. Under ischemia and hypoxia, mitochondria are capable of controlling NLRP3 inflammasome-mediated neuroinflammation through mitochondrial released contents, mitochondrial localization and mitochondrial related proteins. Thus, inflammasome and mitochondria may be attractive targets to treat ischemic stroke as well as the several drugs that target the process of mitochondrial function to treat cerebral ischemic stroke. At present, certain drugs have already been studied in clinical trials.
ISSN:1107-3756
1791-244X
DOI:10.3892/ijmm.2022.5130