Nuevos horizontes para el tratamiento del glaucoma. I : neuroinflamación e inflamasomas

Zanón‐Moreno, Vicente; Raga-Cervera, J.; García-Medina, J.J.; Benítez-del-Castillo, Javier; Vinuesa-Silva, I.; Torregrosa, S.; Pinazo-Durán,

doi:10.1016/j.oftal.2017.11.002

Cited by 7 publications

(4 citation statements)

References 14 publications

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“…Visualization of neuroinflammation in the CNS and eye: In early stages of chronic neurodegenerative and psychiatric diseases, neuroinflammatory mechanisms initiated by chronic activation of innate immunity alter function and trigger death. As microglial alterations (dynamic changes in density and activation) are detectable in early stages of disease and precede neurodegeneration, they have been established as diagnostic and therapeutic biomarkers of progression [ 61 , 91 ]. Direct visualization of the recruitment of specific immune cells from the periphery to the brain [ 57 ] currently requires expensive and invasive techniques such as 2-photon microscopy (T cells), MRI (macrophages) and PET and SPECT (microglia).…”

Section: Discussionmentioning

confidence: 99%

Analysis of Parainflammation in Chronic Glaucoma Using Vitreous-OCT Imaging

et al. 2021

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Glaucoma causes blindness due to the progressive death of retinal ganglion cells. The immune response chronically and subclinically mediates a homeostatic role. In current clinical practice, it is impossible to analyse neuroinflammation non-invasively. However, analysis of vitreous images using optical coherence tomography detects the immune response as hyperreflective opacities. This study monitors vitreous parainflammation in two animal models of glaucoma, comparing both healthy controls and sexes over six months. Computational analysis characterizes in vivo the hyperreflective opacities, identified histologically as hyalocyte-like Iba-1+ (microglial marker) cells. Glaucomatous eyes showed greater intensity and number of vitreous opacities as well as dynamic fluctuations in the percentage of activated cells (50–250 microns2) vs. non-activated cells (10–50 microns2), isolated cells (10 microns2) and complexes (>250 microns2). Smaller opacities (isolated cells) showed the highest mean intensity (intracellular machinery), were the most rounded at earlier stages (recruitment) and showed the greatest change in orientation (motility). Study of vitreous parainflammation could be a biomarker of glaucoma onset and progression.

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Section: Discussionmentioning

confidence: 99%

Analysis of Parainflammation in Chronic Glaucoma Using Vitreous-OCT Imaging

et al. 2021

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“…In the present work, a decrease in VEGF tear expression in the POAG patients respect to the controls was found as expected. OS also plays a principal role in the activation of intracellular sensors, in order to defend the cells from damaging agents, the inflammasomes [67,68]. For addressing the role of INF in the pathogenesis of POAG, tears, aqueous humor, and blood samples were used to identify inflammatory biomarkers for glaucoma.…”

Section: Discussionmentioning

confidence: 99%

“…Neurodegeneration is a hallmark in POAG. Some relevant pathways induce upregulation of proapoptotic gene expression, and in turn, downregulation of neuroprotective factors [68]. Neurotrophins are involved in the survival of neurons and neuroglial cells.…”

Section: Discussionmentioning

confidence: 99%

Computational Analysis of Clinical and Molecular Markers and New Theranostic Possibilities in Primary Open-Angle Glaucoma

Pinazo-Durán

García-Medina

Bolarín

et al. 2020

JCM

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Primary open-angle glaucoma (POAG) is a paramount cause of irreversible visual disability worldwide. We focus on identifying clinical and molecular facts that may help elucidating the pathogenic mechanisms of the disease. By using ophthalmological approaches (biomicroscopy, ocular fundus, optical coherence tomography, and perimetry) and experimental tests (enzyme-linked immunosorbent assay (ELISA), high performance liquid chromatography (HPLC), and Western blot/immunoblotting) directed to evaluate the oxidative stress, inflammation, apoptosis, and neurodegeneration processes, we gather information to build a network of data to perform a computational bioinformatics analysis. Our results showed strong interaction of the above players and its downstream effectors in POAG pathogenesis. In conclusion, specific risk factors were identified, and molecules involved in multiple pathways were found in relation to anterior and posterior eye segment glaucoma changes, pointing to new theranostic challenges for better managing POAG progression.

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“…Parallel to FasL’s downstream actions, TNF-α also triggers RGC cell death [ 77 , 78 ]. In a vitreous glaucoma mouse model, oligodendrocyte and RGC damages are induced by soluble murine TNF-α while TNF-α suppression prevented these damages [ 43 , 79 ]. This is similar to the extent of blocking FasL activity by pharmacotherapy [ 80 ].…”

Section: Main Textmentioning

confidence: 99%

Nanoparticles for the treatment of glaucoma-associated neuroinflammation

et al. 2022

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Recently, a considerable amount of literature has emerged around the theme of neuroinflammation linked to neurodegeneration. Glaucoma is a neurodegenerative disease characterized by visual impairment. Understanding the complex neuroinflammatory processes underlying retinal ganglion cell loss has the potential to improve conventional therapeutic approaches in glaucoma. Due to the presence of multiple barriers that a systemically administered drug has to cross to reach the intraocular space, ocular drug delivery has always been a challenge. Nowadays, studies are focused on improving the current therapies for glaucoma by utilizing nanoparticles as the modes of drug transport across the ocular anatomical and physiological barriers. This review offers some important insights on the therapeutic advancements made in this direction, focusing on the use of nanoparticles loaded with anti-inflammatory and neuroprotective agents in the treatment of glaucoma. The prospect of these novel therapies is discussed in relation to the current therapies to alleviate inflammation in glaucoma, which are being reviewed as well, along with the detailed molecular and cellular mechanisms governing the onset and the progression of the disease.

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Nuevos horizontes para el tratamiento del glaucoma. I : neuroinflamación e inflamasomas

Cited by 7 publications

References 14 publications

Analysis of Parainflammation in Chronic Glaucoma Using Vitreous-OCT Imaging

Analysis of Parainflammation in Chronic Glaucoma Using Vitreous-OCT Imaging

Computational Analysis of Clinical and Molecular Markers and New Theranostic Possibilities in Primary Open-Angle Glaucoma

Nanoparticles for the treatment of glaucoma-associated neuroinflammation

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