ReviewMolecular neurobiology2026
AMPK-NLRP3 Inflammasome Crosstalk: Structural Insights, Molecular Mechanisms, and Therapeutic Implications for Inflammation and Neuroinflammation.
Review in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nucleotide-binding domain leucine-rich repeat and pyrin domain-containing protein-3 (NLRP3) inflammasome plays a central role in inflammatory diseases, including cardiovascular, gastrointestinal, neurodegenerative, autoimmune, hepatic, renal, and pulmonary disorders. Although various cellular pathways tightly regulate its activation, the precise mechanisms remain unclear. Emerging evidence highlights adenosine monophosphate-activated protein kinase (AMPK) as a critical regulator of energy balance and cellular metabolism, suggesting its potential involvement in modulating NLRP3 inflammasome activity. This review explores the structural dynamics of the NLRP3 inflammasome and the activation of AMPK signaling. It focuses on the mechanistic pathways underlying AMPK-mediated suppression of the NLRP3 inflammasome, including autophagy-dependent regulation, sirtuin-mediated regulation, ER stress/TXNIP signaling pathway, regulation of mitochondrial homeostasis, NF-κB/MyD88-mediated priming, and maintenance of lysosomal integrity. Furthermore, the review discusses the interplay of these pathways in CNS-specific disease models, such as Ischemic stroke/cerebral ischemia, Alzheimer's disease, Parkinson's disease, multiple sclerosis, diabetic neuropathy, and neuroinflammation models, as well as traumatic brain injury, streptozotocin-induced neuroinflammation, and lipopolysaccharide-induced neuroinflammation. Additionally, this review examined therapeutic strategies targeting the AMPK-NLRP3 axis in neuroinflammatory and neurodegenerative disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.