| NLRP3 inflammasome: A key player in neonatal brain injury |
Cagla Kiser1,2 
, Ilkcan Ercan1, Defne Engur3, Sermin Genc1,2,4
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1Izmir Biomedicine and Genome Center, Dokuz Eylul University Health Campus, Izmir, Turkey
2Izmir International Biomedicine and Genome Institute, Dokuz Eylul University, Izmir, Turkey
3Department of Neonatology, Izmir Faculty of Medicine, University of Health Sciences, Izmir, Turkey
4Department of Neuroscience, Health Sciences Institute, Dokuz Eylul University, Izmir, Turkey |
Correspondence:
Sermin Genc, Email: sermin.genc@deu.edu.tr
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Received: 13 December 2024 • Revised: 27 February 2025 • Accepted: 4 March 2025 |
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| Abstract |
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Among neonates, hypoxic-ischemic encephalopathy is the most significant cause of mortality and hypoxia-ischemia is among the leading causes of brain damage. The microglia are primary mediators of neuroinflammation. NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation is the first line of defense in the central nervous system. Numerous studies have shown that the NLRP3 inflammasome is activated and pro-inflammatory cytokines are upregulated upon hypoxia-ischemia–induced brain damage. However, aberrant activation of the NLRP3 inflammasome results in cell death and brain tissue damage. Given that neonates are particularly vulnerable to neuroinflammation, which may cause lifelong disabilities, it is important to target the pathways involved in its complex nature to improve their prognosis. The potential use of compounds or drugs that target inflammasome activation to relieve hypoxia-induced brain damage has become significant. This review describes the NLRP3 inflammasome in neonates to contribute to the development of therapeutic approaches. |
| Key Words:
NLRP3 inflammasome, Neonatal, Brain injury, Hypoxia |
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