Journal Article

DZNE-2026-00974

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png NLRP3 Regulation in Neonatal Hypoxic-Ischemic Encephalopathy-Focus on Microglial Activation.

Burkard, H. (First author)DZNE* ; Bernis, M. E.DZNE* ; Bremer, A.-S.DZNE* ; Maes, E.DZNE* ; Walter, J. ; Meissner, F. ; Sabir, H. (Last author)DZNE*

2026
Molecular Diversity Preservation International Basel

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Please use a persistent id in citations: doi:10.3390/ijms27177853

Abstract: Neonatal hypoxic-ischemic encephalopathy (HIE) is a major cause of neonatal mortality and long-term neurological disability, affecting 1-3 per 1000 live births in developed countries and occurring at substantially higher rates in developing countries. Neuroinflammation is a key contributor to disease progression, with growing evidence implicating the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome following hypoxic-ischemic (HI) injury. In this study, we investigated the role and regulation of the NLRP3 inflammasome in neonatal HIE using in vitro and in vivo models. Primary microglial cultures subjected to oxygen-glucose deprivation and the Vannucci neonatal rat model of HI were used to characterize NLRP3 activation and its contribution to injury. We demonstrated that HI induces NLRP3 inflammasome activation, whereas pharmacological inhibition of NLRP3 enhances cell viability and attenuates brain damage. Our findings identify microglia as a central mediator of NLRP3-driven neuroinflammation and highlight microglial NLRP3 signaling as a promising therapeutic target for neuroinflammatory diseases. Collectively, this study provides an integrated view of NLRP3 regulation in neonatal HIE and supports inflammasome-directed strategies for neuroprotection following neonatal HI injury.

Keyword(s): NLR Family, Pyrin Domain-Containing 3 Protein: metabolism (MeSH) ; NLR Family, Pyrin Domain-Containing 3 Protein: genetics (MeSH) ; Animals (MeSH) ; Microglia: metabolism (MeSH) ; Microglia: pathology (MeSH) ; Hypoxia-Ischemia, Brain: metabolism (MeSH) ; Hypoxia-Ischemia, Brain: pathology (MeSH) ; Animals, Newborn (MeSH) ; Rats (MeSH) ; Inflammasomes: metabolism (MeSH) ; Signal Transduction (MeSH) ; Disease Models, Animal (MeSH) ; Rats, Sprague-Dawley (MeSH) ; Humans (MeSH) ; Cells, Cultured (MeSH) ; glia cells ; inflammation ; neurodevelopmental outcomes ; new therapeutic option ; newborn brain injury ; NLR Family, Pyrin Domain-Containing 3 Protein ; Inflammasomes ; Nlrp3 protein, rat

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Contributing Institute(s):

1. Neonatal Neuroscience (AG Sabir)

Research Program(s):

1. 352 - Disease Mechanisms (POF4-352) (POF4-352)

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Database coverage:
; Clarivate Analytics Master Journal List ; Current Contents - Physical, Chemical and Earth Sciences ; Ebsco Academic Search ; Essential Science Indicators ; IF >= 5 ; JCR ; PubMed Central ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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