ReviewNeuroimmunomodulation2026
NLRP3 Inflammasome Activation in Oxidative Stress: A Key Mechanism Driving Neuroinflammation.
Review in Neuroimmunomodulation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn acquired and neurodegenerative brain diseases, inflammation-mediated neuronal death contributes to the deterioration of neurological deficits in patients. In the innate immune system, the NLRP3 inflammasome is a cytosolic complex that regulates the release of proinflammatory cytokines IL-1β and IL-18, thereby amplifying the inflammatory response and neuronal damage. Consequently, inhibition of the NLRP3 inflammasome represents a promising pharmacological strategy to limit inflammation across multiple pathologies. Oxidative stress is a common hallmark of these pathological conditions that contribute to neuronal death and influence NLRP3 activation. Despite the implications of these events, the molecular mechanisms underlying this activation remain poorly understood. SUMMARY: In this review, we describe the key features of the NLRP3 inflammasome and explore the role of oxidative stress in its activation. Additionally, we discuss the evidence supporting the regulation of inflammasome activity by antioxidant molecules. KEY MESSAGE: Understanding the role of oxidative stress in NLRP3-mediated inflammation offers promising advantages for therapeutic strategies to reduce neuronal death.
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