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Retinopathy of prematurity: contribution of inflammatory and genetic factors

dc.contributor.authorFevereiro-Martins, M
dc.contributor.authorGuimarães, H
dc.contributor.authorMarques-Neves, C
dc.contributor.authorBicho, M
dc.date.accessioned2024-10-02T20:18:57Z
dc.date.available2024-10-02T20:18:57Z
dc.date.issued2022
dc.description.abstractRetinopathy of prematurity (ROP) is a retinal vasoproliferative disorder that represents an important cause of childhood visual impairment and blindness. Although oxidative stress has long been implicated in ROP etiology, other prenatal and perinatal factors are also involved. This review focuses on current research involving inflammation and genetic factors in the pathogenesis of ROP. Increasing evidence suggests that perinatal inflammation or infection contributes to ROP pathogenesis. Cytokines and chemokines with a fundamental role in inflammatory responses and that significantly contributing to angiogenesis are analyzed. Microglia cells, the retinal-resident macrophages, are crucial for retinal homeostasis, however, under sustained pathological stimuli release exaggerated amounts of inflammatory mediators and can promote pathological neovascularization. Current modulation of angiogenic cytokines, such as treatment with antibodies to vascular endothelial growth factor (anti-VEGF), has shown efficacy in the treatment of ocular neovascularization; however, some patients are refractory to anti-VEGF agents, suggesting that other angiogenic or anti-angiogenic cytokines need to be identified. Much evidence suggests that genetic factors contribute to the phenotypic variability of ROP. Several studies have implicated the involvement of candidate genes from different signaling pathways in the development of ROP. However, a genetic component with a major impact on ROP has not yet been discovered. Most studies have limitations and did not replicate results. Future research involving bioinformatics, genomics, and proteomics may contribute to finding more genes associated with ROP and may allow discovering better solutions in the management and treatment of ROP.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationMol Cell Biochem . 2022 Jun;477(6):1739-1763.pt_PT
dc.identifier.doi10.1007/s11010-022-04394-4pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.26/52374
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.subjectRetinopatia da Prematuridade/genéticapt_PT
dc.subjectRetinopathy of Prematurity/geneticspt_PT
dc.titleRetinopathy of prematurity: contribution of inflammatory and genetic factorspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage1763pt_PT
oaire.citation.issue6pt_PT
oaire.citation.startPage1739pt_PT
oaire.citation.titleMolecular and Cellular Biochemistrypt_PT
oaire.citation.volume477pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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