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Systemic inflammation aggravates retinal ganglion cell vulnerability to optic nerve trauma in adult rats

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dc.contributor.authorRovere, Giuseppe
dc.contributor.authorCaja Matas, Yolanda
dc.contributor.authorVidal Villegas, Beatriz
dc.contributor.authorBernal Garro, José M.
dc.contributor.authorSobrado Calvo, Paloma
dc.contributor.authorSalinas Navarro, Manuel Ángel
dc.contributor.authorNucci, Carlo
dc.contributor.authorVillegas Pérez, Maria Paz
dc.contributor.authorVidal Sanz, Manuel
dc.contributor.authorAgudo Barriuso, Marta
dc.contributor.authorNadal-Nicolás, Francisco Manuel
dc.contributor.departmentOftalmología, Optometría, Otorrinolaringología y Anatomía Patológica
dc.contributor.otherFacultades de la UMU::Facultad de Medicina
dc.date.accessioned2026-02-23T09:46:24Z
dc.date.available2026-02-23T09:46:24Z
dc.date.copyright2026 by the authors. Licensee MDPI, Basel, Switzerland.
dc.date.copyright© 2026 by the authors
dc.date.issued2026-02-03
dc.description.abstractSystemic inflammation is increasingly recognized as a modifier of neurodegenerative outcomes in the central nervous system; however, its impact on retinal ganglion cell (RGC) survival and retinal microglial responses following optic nerve (ON) injury in vivo remains incompletely understood. In this study, we investigated how systemic lipopolysaccharide (LPS)-induced inflammation influences retinal microglial activation and RGC vulnerability under physiological conditions and after traumatic ON damage. In adult female rats, systemic LPS administration by intraperitoneal injection induced rapid and robust microglial activation, characterized by process retraction and soma hypertrophy within hours and promoting microglial proliferation at later stages but without causing RGC loss in intact retinas. Following ON crush, systemic inflammation did not affect early RGC degeneration but significantly exacerbated neuronal loss during the late acute phase. This increased vulnerability was accompanied by a marked rise in microglial density and a pronounced redistribution of microglia toward the central retina and the ON head, a region of heightened anatomical and metabolic susceptibility. Together, these findings demonstrate that, in rats, systemic inflammation alone is insufficient to induce RGC degeneration but acts as a potent priming factor that amplifies neurodegeneration in the context of axonal injury. The temporal and spatial specificity of microglial responses underscores their context-dependent role in retinal pathology and identifies systemic inflammatory status as a critical determinant of retinal outcome after trauma. Targeted, time-dependent modulation of microglial activation may therefore represent a promising therapeutic strategy for optic neuropathies.
dc.formatapplication/pdf
dc.format.extent23
dc.identifier.citationInt. J. Mol. Sci. 2026, 27(3), 1502
dc.identifier.doihttps://doi.org/10.3390/ijms27031502
dc.identifier.urihttp://hdl.handle.net/10201/210181
dc.languageeng
dc.publisherMDPI
dc.relationThis research was funded by the Spanish Ministry of Economy and Competitiveness PID2019-106498GB-I00 MCIN/AEI/10.13039/501100011033 (M.V.-S.), RD16/0008/0026 co-funded by FEDER “A way to make Europe” (M.P.V.-P.), CNS2022-135290 (CdlR), by the Instituto de Salud Carlos III, Fondo Europeo de Desarrollo Regional “A way to make Europe” project: PI24/0040 (M.A.-B.), and by the Fundación Séneca (Murcia, Spain) 22395/SF/23 (F.M.N.-N.) and 23037/GERM/25 (M.P.V.-P.).
dc.relation.publisherversionhttps://www.mdpi.com/1422-0067/27/3/1502
dc.rightsAttribution 4.0 International*
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectTraumatic injury
dc.subjectOptic nerve crush
dc.subjectInflammation
dc.subjectNeuroinflammation
dc.subjectSystemic infection
dc.subjectLipopolysaccharide
dc.subjectAdult albino female rat
dc.subjectMicroglial cells
dc.subjectMicroglia activation
dc.subjectRetina
dc.subject.odsObjetivo 3: Salud
dc.titleSystemic inflammation aggravates retinal ganglion cell vulnerability to optic nerve trauma in adult rats
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dspace.entity.typePublicationes
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