Neuroinflammation as a target for glaucoma therapy

作者:Adornetto Annagrazia;Rossella Russo;Parisi Vincenzo; 刊名:Neural Regeneration Research 上传者:叶春霞

【摘要】The pathogenesis of glaucoma is still not fully clarified but a growing body of evidence suggests that neuroinflammation and immune response are part of the sequence of pathological events leading to the optic neuropathy. Indeed, inflammation-involving the activation and proliferation of resident glial cells(astrocytes, Muller cells and microglia) and the release of a plethora of anti-and pro-inflammatory cytokines, chemokines and reactive oxygen species-has been reported as common features in clinical and experimental glaucoma. In the insulted retina, as for other neuronal tissues, pathogenic and reparative aspects coexist in the inflammatory process, with extent and persistency affecting the final outcome. In view of this, therapies aimed at modulating the immune and inflammatory responses may represent a promising approach for limiting the optic nerve damage and the loss of retinal ganglion cells associated with glaucoma.

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www.nrronline.org 391 NEURAL REGENERATION RESEARCH Neuroinflammation as a target for glaucoma therapy Glaucoma is a group of chronic optic neuropathies, characterized by the alteration of the optic nerve and the death of retinal ganglion cells and represents a leading cause of irreversible blindness, estimated to affect 76 million in 2020 and 112 million people in 2040 (Tham et al., 2014). Age and elevated intraocu-lar pressure are considered major risk factors for the onset and progression of the disease and, accordingly, all the approved therapies aim to intraocular pressure lowering. However, the high incidence of normal tension glaucoma and the recurrence of patients that continue to lose vision even when intraocular pres-sure values are successfully controlled, highlight the fact that elevated intraocular pressure is not sufficient nor necessary for developing the disease (Blumberg et al., 2015). Therefore, alternative treatments, be-yond and/or independent of intraocular pressure reduction, are required to fulfill the need of a better glaucoma therapy. We have performed a PubMed literature search with the key words: glaucoma and neuroinflammation, glaucoma and microglia activa-tion, glaucoma and inflammasome. Over the course of the disease, apoptotic retinal ganglion cell death occurs through a complex se-quence of pathological events that involve several contributing factors (i.e., modifications of neurotro-phin signaling, excitotoxicity, oxidative stress, mito-chondri

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