Inflammatory pathways in pathological neovascularization in retina and choroid: a narrative review on the inflammatory drug target molecules in retinal and choroidal neovascularization

Kim, Soo‐Young; Kim, Young-Hwa; Oh, Youngman

doi:10.21037/aes-21-4

Cited by 7 publications

(5 citation statements)

References 116 publications

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“…Numerous clinical trials have focused on modulating retinal inflammation to promote tissue regeneration, but achieving consistent treatment success has proven challenging. The underlying causes of these failures are unclear (Kim et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Glia-Mediated Antigen Presentation In The Retina During Degeneration

Intonti,

Kokona,

Zinkernagel

et al. 2024

Preprint

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Glia antigen-presenting cells (APCs) are pivotal regulators of immune surveillance within the retina, maintaining tissue homeostasis and promptly responding to insults. The intricate mechanisms underlying their local coordination and activation remain unclear. Our study integrates an animal model of retinal injury, retrospective analysis of human retinas, and in vitro experiments to elucidate insights into the pivotal role of antigen presentation in neuroimmunology during retinal degeneration, uncovering the involvement of various glial cells, notably Muller glia, and microglia. Glial cells act as sentinels, detecting antigens released during degeneration and interacting with T-cells via MHC molecules, which are essential for immune responses. Microglia function as APCs via the MHC class II pathway, upregulating key molecules such as Csf1r and cytokines. In contrast, Muller cells act as atypical APCs through the MHC class I pathway, exhibiting upregulated antigen processing genes and promoting a CD8+ T-cell response. Human retinal specimens corroborate these findings, demonstrating glial activation and MHC expression correlating with degenerative changes. In vitro assays also confirmed differential T-cell migration responses to activated microglia and Muller cells, highlighting their role in shaping the immune milieu within the retina. These insights emphasize the complex interplay between glial cells and T-cells, influencing the inflammatory environment and potentially modulating degenerative processes. In summary, our study emphasizes the involvement of retinal glial cells in modulating the immune response after insults to the retinal parenchyma. Thus, unraveling the intricacies of glia-mediated antigen presentation in retinal degeneration is essential for developing precise therapeutic interventions for retinal pathologies.

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Section: Discussionmentioning

confidence: 99%

Glia-Mediated Antigen Presentation In The Retina During Degeneration

Intonti,

Kokona,

Zinkernagel

et al. 2024

Preprint

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“…Inflammatory signaling pathways are highly active in ocular settings, which results in a wide range of ocular inflammatory diseases, including DR and nAMD (Kim et al, 2021). Prolonged and exacerbated local inflammation in the eyes is directly or indirectly a major cause of vision impairment or blindness.…”

Section: New Targets (Non-vegf) In Clinical Trials: Links To Inflamma...mentioning

confidence: 99%

“…Multiple signaling pathways such as the complement pathway, stromal derived factor-1 (SDF-1)/chemokine CXC receptor-4 (CXCR4), inflammasome nucleotidebinding oligomerization domain-like receptor containing domain 3 (NLRP3), interleukin 18 (IL-18), programed cell death ligand-1 (PD-L1), insulin-like growth factor (IGF) and Yes-associated protein (YAP) signaling pathways were recently implicated in the pathogenesis of DR, nAMD and ocular inflammation (Wu et al, 2017;Yan et al, 2018;Yerramothu, 2018;Kim et al, 2021). However, some of these signaling pathways work together with upstream or downstream effectors of VEGF signaling to some extent, such as the complement pathway, transforming growth factor- (TGF-β) signaling, as well as activation of crucial oncogenic transcriptional factors (TFs) such as NF-B and STAT3 (Wang et al, 2017;Sardar Pasha et al, 2018;Dong et al, 2020).…”

Section: New Targets (Non-vegf) In Clinical Trials: Links To Inflamma...mentioning

confidence: 99%

Beyond VEGF: Targeting Inflammation and Other Pathways for Treatment of Retinal Disease

Anbukkarasi

Hartman

Yang

et al. 2023

J Pharmacol Exp Ther

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Downloaded fromassociated protein kinase; ROP, retinopathy of prematurity; ROS, reactive oxygen species; RPE, retinal pigment epithelium; RUNX1, runt-related transcription factor 1; sEH, soluble epoxide hydrolase; SDF-1, stromal derived factor-1; shRNA, small hairpin RNA; STAT3, signal transducer and activator of transcription 3; t-AUCB, trans-4-(4-(3adamantan-1-yl-ureido)-cyclohexyloxy)-benzoic acid; TF, transcription factor; Tff1, trefoil factor family 1; TGF-β2, transforming growth factor-β2; TNF-α, tumor necrosis factoralpha; TPPU, 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea; VEGF, vascular endothelial growth factor; VEGFR2, vascular endothelial growth factor receptor 2; YAP, yes-associated protein.

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“…Кроме того, следует иметь в виду, что при ВМД могут иметь место схожие с сотовидной дистрофией механизмы друзообразования. Ведь известно, что ВМД, согласно современным представлениям, относится к нейродегенеративным заболеваниям глаз с относительно частой ассоциацией с другими нейродегенеративными заболеваниями [45][46][47]; в развитии патологических изменений на глазном дне при ВМД имеет место заинтересованность нервных волокон хориоидальных сосудов и клеточных элементов сетчатки и хориоидеи нейрального происхождения [48][49][50][51]; были получены положительные результаты нейропротекторной терапии при ВМД [52,53].…”

Section: клинический случайunclassified

Familial Dominant Drusen: Novel Data on Pathogenesis (Literature Review and Clinical Case Presentation)

Велиева

2023

Офтальмология. Восточная Европа

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Наследственные доминантные друзы (сотовидная дистрофия сетчатки Дойна) – это генетически обусловленное заболевание сетчатки с вариабельной клинической картиной. Изучение этиопатогенеза сотовидной дистрофии затруднительно ввиду низкой частоты встречаемости этой нозологии. Под нашим наблюдением находилась пациентка К., 68 лет, обратившаяся с подозрением на нормотензивную глаукому обоих глаз. По итогам офтальмологического обследования был верифицирован диагноз «доминантные друзы», а также было установлено, что дефекты поля зрения, возникающие при этом заболевании, обусловлены истончением комплекса ганглиозных клеток и нервных волокон сетчатки. Приведенный в настоящей статье анализ литературы и клинического случая позволил расширить представление о механизмах нарушения зрительных функций при сотовидной дистрофии. Familial dominant drusen (Doyne honeycomb retinal dystrophy) – is genetically determined retinal disease with variable clinical manifestations. Honeycomb dystrophy etiology and pathogenesis are difficult to research due to low incidence of the disease. Here in the article we present a clinical observation of a female 68 years old patient K., who was initially suspected for low-tension glaucoma in both eyes. Ophthalmologic examination revealed dominant drusen; as well, ganglion cell complex and retinal nerve fibers thinning was found to be the source of visual field defects arising from the disease. The clinical case and literature review presented in the article adds to our knowledge of visual impairment mechanisms in honeycomb dystrophy.

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Inflammatory pathways in pathological neovascularization in retina and choroid: a narrative review on the inflammatory drug target molecules in retinal and choroidal neovascularization

Cited by 7 publications

References 116 publications

Glia-Mediated Antigen Presentation In The Retina During Degeneration

Glia-Mediated Antigen Presentation In The Retina During Degeneration

Beyond VEGF: Targeting Inflammation and Other Pathways for Treatment of Retinal Disease

Familial Dominant Drusen: Novel Data on Pathogenesis (Literature Review and Clinical Case Presentation)

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