Journal ArticleDOI
Pathogenesis of acute stroke and the role of inflammasomes
David Y. Fann,Seung-Yoon Lee,Silvia Manzanero,Prasad Chunduri,Christopher G. Sobey,Thiruma V. Arumugam,Thiruma V. Arumugam +6 more
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TLDR
The molecular structure, cellular signaling pathways and current evidence for inflammasome activation following cerebral ischemia, and the potential for future treatments for stroke that may involve targeting inflammaome formation or its products in the ischemic brain are described.About:
This article is published in Ageing Research Reviews.The article was published on 2013-09-01. It has received 258 citations till now. The article focuses on the topics: NLRP6 & Inflammasome.read more
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Hallmarks of Brain Aging: Adaptive and Pathological Modification by Metabolic States.
TL;DR: An overview of the cellular and molecular biology of brain aging, how those processes interface with disease-specific neurodegenerative pathways, and how metabolic states influence brain health is provided.
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Functions and mechanisms of microglia/macrophages in neuroinflammation and neurogenesis after stroke
TL;DR: This review summarizes recent progress concerning the mechanisms involved in brain damage, repair and regeneration related to microglia/macrophage activation and phenotype transition after stroke and argues that future translational studies should be targeting multiple key regulating molecules to improve brain repair.
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Self-regulation and cross-regulation of pattern-recognition receptor signalling in health and disease
Xuetao Cao,Xuetao Cao +1 more
TL;DR: In this Review, many of the numerous distinct mechanisms for the self-regulation and cross-regulation of innate immune receptor signalling are described.
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Oxidative stress in obstructive sleep apnea and intermittent hypoxia--revisited--the bad ugly and good: implications to the heart and brain.
TL;DR: In this article, the authors present the currently available data on redox biology in physiological/pathophysiological conditions and in OSA/IH, in order to better understand the apparently contradictory findings on damage vs. repair.
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NLRP3 Inflammasome in Neurological Diseases, from Functions to Therapies.
TL;DR: A series of promising therapeutic approaches that target theNLRP3 inflammasome signaling including anti-IL-1 therapy, small molecule NLRP3 inhibitors and other compounds are reviewed, however, these approaches are still experimental in neurological diseases.
References
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NOD-like receptors and the innate immune system: coping with danger, damage and death.
TL;DR: The roles of NLR family members in health and disease are reviewed, with emphasis on the signaling mechanisms in cell death and inflammation.
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Fundamental role of the Rip2/caspase-1 pathway in hypoxia and ischemia-induced neuronal cell death.
Wenhua Zhang,Xin Wang,Malini V. Narayanan,Yu Zhang,Chunfeng Huo,John C. Reed,Robert M. Friedlander +6 more
TL;DR: It is demonstrated that caspase-1 is an apical mediator of neuronal cell death during in vitro hypoxia and confirmed in vivo in ischemia, and insights are provided into the sequence of events involved in this pathological cell death process.
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Acidic environment causes apoptosis by increasing caspase activity.
TL;DR: The finding in the present study demonstrated that acidic intra-tumour environment may markedly perturb the tumour cell proliferation and tumour growth.
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Glutathione s-transferase omega 1-1 is a target of cytokine release inhibitory drugs and may be responsible for their effect on interleukin-1beta posttranslational processing.
Ronald E. Laliberte,David G. Perregaux,Lise R. Hoth,Philip J. Rosner,Crystal K. Jordan,Kevin M. Peese,James F. Eggler,Mark A. Dombroski,Kieran F. Geoghegan,Christopher A. Gabel +9 more
TL;DR: The ability of CRIDs to arrest stimulus-induced IL-1β posttranslational processing may be attributable to their interaction with glutathioneS-transferase (GST) Omega 1-1.
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Excitotoxic brain damage in the rat induces interleukin-1beta protein in microglia and astrocytes: correlation with the progression of cell death.
TL;DR: This work has investigated the expression of IL‐1β protein by glial cells in vivo in response to NMDA receptor‐mediated excitotoxicity in the rat parietal cortex and striatum.