Khiany Mathias, Richard Simon Machado, Taise Cardoso, Beatriz Naspolini, Josiane Prophiro, Fabricia Petronilho
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引用次数: 0
Abstract
Neonatal hypoxic-ischemic (HI) injury is a critical condition associated with significant acute brain damage and long-term neurological impairments. Growing evidence highlights the role of the NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome, a key multiprotein complex driving neuroinflammation, in the progression of neonatal HI brain injury. Activation of the NLRP3 inflammasome triggers the release of pro-inflammatory cytokines, including interleukin-1 beta (IL-1β), which plays a pivotal role in exacerbating brain damage. This article examines current research to better understand the relationship between neonatal HI, NLRP3 inflammasome activation, and neuroinflammatory process. Furthermore, it emphasizes the therapeutic potential of targeting this pathway, proposing its modulation as a promising neuroprotective strategy to reduce neuroinflammation and improve outcomes in affected neonates.
期刊介绍：
NeuroMolecular Medicine publishes cutting-edge original research articles and critical reviews on the molecular and biochemical basis of neurological disorders. Studies range from genetic analyses of human populations to animal and cell culture models of neurological disorders. Emerging findings concerning the identification of genetic aberrancies and their pathogenic mechanisms at the molecular and cellular levels will be included. Also covered are experimental analyses of molecular cascades involved in the development and adult plasticity of the nervous system, in neurological dysfunction, and in neuronal degeneration and repair. NeuroMolecular Medicine encompasses basic research in the fields of molecular genetics, signal transduction, plasticity, and cell death. The information published in NEMM will provide a window into the future of molecular medicine for the nervous system.
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