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IJMS
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Age-Related Macular Degeneration and Diabetic Retinopathy
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Age-Related Macular Degeneration and Diabetic Retinopathy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (28 December 2023) | Viewed by 6975

Special Issue Editor

Dr. Jay Stewart

E-Mail Website
Guest Editor
Department of Ophthalmology, University of California, San Francisco, CA 94158, USA
Interests: age-related macular degeneration; diabetic retinopathy; retinal detachment

Special Issue Information

Dear Colleagues, 

This Special Issue of IJMS focuses on two critical eye diseases affecting the vision of millions across the globe: Age-Related Macular Degeneration (AMD) and Diabetic Retinopathy (DR). Both of these conditions entail a complex pathogenesis that can depend upon contributions from a patient’s genetic background as well as other systemic factors that determine the microenvironment at the back of the eye. The retina and other posterior ocular structures are affected by biochemical and molecular pathways that may show some overlap with other parts of the body but that often have unique features that decisively impact the manifestation of processes including senescence, microvasculopathy, and inflammation, among others, and their direct correlation to the stability and functioning of the visual system. Through this special issue, we aim to feature important contributions to the literature that can advance our understanding of the basic processes and pathways that underlie these two important vision-threatening conditions. It is our hope that by furthering knowledge about the key molecular aspects of these diseases, this Special Issue of IJMS can help to open up new avenues of research and facilitate the development of novel therapeutic approaches in ophthalmology. We encourage submissions exploring biomolecular research in AMD and DR from investigators proposing novel ideas and methods that can help strengthen these essential areas of vision research.

Dr. Jay Stewart
Guest Editor

Manuscript Submission Information

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Keywords

  • age-related macular degeneration
  • drusen
  • retinal pigment epithelium
  • geographic atrophy
  • complement, choroidal neovascularization
  • retina
  • macula
  • diabetic retinopathy
  • cytokines
  • vitreous
  • retina
  • vascular endothelial growth factor
  • inflammation
  • macular edema
  • vitreous hemorrhage
  • traction retinal detachment

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Published Papers (3 papers)

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Research

20 pages, 2971 KiB  
Article
Intravitreal Metformin Protects Against Choroidal Neovascularization and Light-Induced Retinal Degeneration
by Jason F. Xiao, Wendy Luo, Amir Mani, Hugo Barba, Aniruddhsingh Solanki, Steven Droho, Jeremy A. Lavine and Dimitra Skondra
Int. J. Mol. Sci. 2024, 25(21), 11357; https://doi.org/10.3390/ijms252111357 - 22 Oct 2024
Viewed by 3445
Abstract
Neovascular age-related macular degeneration (nAMD), a leading cause of blindness in older adults, presents a challenging pathophysiology involving choroidal neovascularization (CNV) and retinal degeneration. Current treatments relying on intravitreal (IVT) administration of anti-angiogenic agents are costly and of moderate effectiveness. Metformin, the common [...] Read more.
Neovascular age-related macular degeneration (nAMD), a leading cause of blindness in older adults, presents a challenging pathophysiology involving choroidal neovascularization (CNV) and retinal degeneration. Current treatments relying on intravitreal (IVT) administration of anti-angiogenic agents are costly and of moderate effectiveness. Metformin, the common anti-diabetic drug, has been associated with decreased odds of developing AMD. Studies have shown that metformin can mitigate cellular aging, neoangiogenesis, and inflammation across multiple diseases. This preclinical study assessed metformin’s impact on vessel growth using choroidal explants before exploring IVT metformin’s effects on laser-induced CNV and light-induced retinal degeneration in C57BL/6J and BALB/cJ mice, respectively. Metformin reduced new vessel growth in choroidal explants in a dose-dependent relationship. Following laser induction, IVT metformin suppressed CNV and decreased peripheral infiltration of IBA1+ macrophages/microglia. Furthermore, IVT metformin protected against retinal thinning in response to light-induced degeneration. IVT metformin downregulated genes in the choroid and retinal pigment epithelium which are associated with angiogenesis and inflammation, two key processes that drive nAMD progression. These findings underscore metformin’s capacity as an anti-angiogenic and neuroprotective agent, demonstrating this drug’s potential as an accessible option to help manage nAMD. Full article
(This article belongs to the Special Issue Age-Related Macular Degeneration and Diabetic Retinopathy)
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14 pages, 1274 KiB  
Article
Systemic Evidence for Mitochondrial Dysfunction in Age-Related Macular Degeneration as Revealed by mtDNA Copy Number Measurements in Peripheral Blood
by Adriana Koller, Claudia Lamina, Caroline Brandl, Martina E. Zimmermann, Klaus J. Stark, Hansi Weissensteiner, Reinhard Würzner, Iris M. Heid and Florian Kronenberg
Int. J. Mol. Sci. 2023, 24(22), 16406; https://doi.org/10.3390/ijms242216406 - 16 Nov 2023
Cited by 3 | Viewed by 1712
Abstract
Mitochondrial dysfunction is a common occurrence in the aging process and is observed in diseases such as age-related macular degeneration (AMD). Increased levels of reactive oxygen species lead to damaged mitochondrial DNA (mtDNA), resulting in dysfunctional mitochondria, and, consequently, mtDNA causes further harm [...] Read more.
Mitochondrial dysfunction is a common occurrence in the aging process and is observed in diseases such as age-related macular degeneration (AMD). Increased levels of reactive oxygen species lead to damaged mitochondrial DNA (mtDNA), resulting in dysfunctional mitochondria, and, consequently, mtDNA causes further harm in the retinal tissue. However, it is unclear whether the effects are locally restricted to the high-energy-demanding retinal pigment epithelium or are also systematically present. Therefore, we measured mtDNA copy number (mtDNA-CN) in peripheral blood using a qPCR approach with plasmid normalization in elderly participants with and without AMD from the AugUR study (n = 2262). We found significantly lower mtDNA-CN in the blood of participants with early (n = 453) and late (n = 170) AMD compared to AMD-free participants (n = 1630). In regression analyses, we found lower mtDNA-CN to be associated with late AMD when compared with AMD-free participants. Each reduction of mtDNA-CN by one standard deviation increased the risk for late AMD by 24%. This association was most pronounced in geographic atrophy (OR = 1.76, 95% CI 1.19–2.60, p = 0.004), which has limited treatment options. These findings provide new insights into the relationship between mtDNA-CN in blood and AMD, suggesting that it may serve as a more accessible biomarker than mtDNA-CN in the retina. Full article
(This article belongs to the Special Issue Age-Related Macular Degeneration and Diabetic Retinopathy)
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17 pages, 4245 KiB  
Article
The Slow Progression of Diabetic Retinopathy Is Associated with Transient Protection of Retinal Vessels from Death
by Yanliang Li, Basma Baccouche, Norma Del-Risco, Jason Park, Amy Song, J. Jason McAnany and Andrius Kazlauskas
Int. J. Mol. Sci. 2023, 24(13), 10869; https://doi.org/10.3390/ijms241310869 - 29 Jun 2023
Cited by 4 | Viewed by 1354
Abstract
The purpose of this study was to investigate the reason that diabetic retinopathy (DR) is delayed from the onset of diabetes (DM) in diabetic mice. To this end, we tested the hypothesis that the deleterious effects of DM are initially tolerated because endogenous [...] Read more.
The purpose of this study was to investigate the reason that diabetic retinopathy (DR) is delayed from the onset of diabetes (DM) in diabetic mice. To this end, we tested the hypothesis that the deleterious effects of DM are initially tolerated because endogenous antioxidative defense is elevated and thereby confers resistance to oxidative stress-induced death. We found that this was indeed the case in both type 1 DM (T1D) and type 2 DM (T2D) mouse models. The retinal expression of antioxidant defense genes was increased soon after the onset of DM. In addition, ischemia/oxidative stress caused less death in the retinal vasculature of DM versus non-DM mice. Further investigation with T1D mice revealed that protection was transient; it waned as the duration of DM was prolonged. Finally, a loss of protection was associated with the manifestation of both neural and vascular abnormalities that are diagnostic of DR in mice. These observations demonstrate that DM can transiently activate protection from oxidative stress, which is a plausible explanation for the delay in the development of DR from the onset of DM. Full article
(This article belongs to the Special Issue Age-Related Macular Degeneration and Diabetic Retinopathy)
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