Connexin and Pannexin Hemichannels: Broad-Spectrum Players in Neuroinflammatory Signaling

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dc.catalogadorjlo
dc.contributor.authorSáez, Juan C.
dc.contributor.authorOcaranza, Francisco J.
dc.contributor.authorPrieto‐Villalobos, Juan
dc.contributor.authorOrellana, Juan A.
dc.date.accessioned2025-09-29T14:03:58Z
dc.date.available2025-09-29T14:03:58Z
dc.date.issued2025
dc.description.abstractConnexin- and pannexin-formed hemichannels have emerged as pivotal, upstream amplifiers of neuroinflammation. Under physiological stressors—depolarization, Ca2+ overload, redox shift, or cytokine exposure—these large pores release adenosine triphosphate, glutamate, and other danger signals that activate P2X/P2Y and N-methyl-D-aspartate receptors, ignite NLR family pyrin domain containing (NLRP) 3 inflammasome, and propagate Ca2+/reactive oxygen species waves between mast cells, microglia, astrocytes, oligodendrocytes, neurons, and brain endothelium. Evidence across acute (e.g., stroke, trauma, seizure, and sepsis) and chronic (e.g., Alzheimer's, and multiple sclerosis) models shows that genetic ablation or pharmacological blockade of hemichannels shrinks lesions, preserves synaptic plasticity, restores blood–brain barrier integrity, and rescues cognition, often without altering the primary pathogenic trigger. Translational leads include mimetic peptides (e.g., Gap19, 10panx1), the nanomolar, gap junction–sparing small-molecule D4, and the pleiotropic alkaloid boldine, all of which curb epileptiform activity, neurodegeneration, and depressive-like behavior. Yet key gaps persist, such as the long-term safety of chronic inhibition, which remains poorly defined and will be critical to translate these “gatekeeper” channels into next-generation neuro–anti-inflammatory therapeutics.
dc.format.extent24 páginas
dc.fuente.origenORCID
dc.identifier.doi10.1111/jnc.70237
dc.identifier.eissn1471-4159
dc.identifier.urihttps://doi.org/10.1111/jnc.70237
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/105802
dc.information.autorucEscuela de Medicina; Prieto Villalobos, Juan Carlos; S/I; 1071673
dc.information.autorucEscuela de Medicina; Carrasco Orellana, Juan Andrés; S/I; 85824
dc.issue.numero9
dc.language.isoen
dc.nota.accesocontenido parcial
dc.revistaJournal of Neurochemistry
dc.rightsacceso restringido
dc.subjectConnexins
dc.subjectGlia
dc.subjectHemichannels
dc.subjectNeuroinflammation
dc.subjectNeurons
dc.subjectPannexins
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.titleConnexin and Pannexin Hemichannels: Broad-Spectrum Players in Neuroinflammatory Signaling
dc.typeartículo
dc.volumen169
sipa.codpersvinculados1071673
sipa.codpersvinculados85824
sipa.trazabilidadORCID;2025-09-22
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