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Journal ArticleDOI

Pathogenesis of acute stroke and the role of inflammasomes

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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.
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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.

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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

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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Inflammasome activation in NADPH oxidase defective mononuclear phagocytes from patients with chronic granulomatous disease

TL;DR: Phagocyte oxidase defective monocytes are identified as a source of elevated IL-1 and provide a potential therapeutic option to ameliorate inflammatory conditions associated with CGD.
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Prolonged activation of ASIC1a and the time window for neuroprotection in cerebral ischaemia

TL;DR: The neuroprotective time window for ASIC1a blockade in a mouse model of focal ischaemia is examined and the role of acidosis per se addressed by continuous pH measurements in penumbral cortex and post-ischaemic alkalization of brain is addressed.
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Chronic Interleukin-1β Expression in Mouse Brain Leads to Leukocyte Infiltration and Neutrophil-Independent Blood–Brain Barrier Permeability without Overt Neurodegeneration

TL;DR: Surprisingly, neutrophils were observed in the hippocampal parenchyma as late as 1 year after transgene induction, coincident with upregulation of the potent neutrophil chemotactic chemokines KC (keratinocyte-derived chemokine) and MIP-2 (macrophage inflammatory protein 2) (CXCL2).
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Synergy of IL-12 and IL-18 for IFN-γ Gene Expression: IL-12-Induced STAT4 Contributes to IFN-γ Promoter Activation by Up-Regulating the Binding Activity of IL-18-Induced Activator Protein 1

TL;DR: Results show that STAT4 up-regulates AP-1-mediated IFn-γ promoter activation without directly binding to the promoter sequence, providing a mechanistic explanation for IL-12/IL-18-induced synergistic enhancement of IFN-γ gene expression.
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Inhibition of ischaemic hippocampal neuronal death in primates with cathepsin B inhibitor CA‐074: a novel strategy for neuroprotection based on ‘calpain–cathepsin hypothesis’

TL;DR: In this article, micro-calpain activation at the disrupted lysosomal membrane of postischaemic Cornu Ammonis (CA) neurons in the monkey undergoing a complete 20 min whole brain ischaemia was demonstrated.
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