NLRP3 inflammasome: a key player in neonatal brain injury.

Abstract

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 proinflammatory 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.