The Role of Inflammation in AMD (Multifactorial Age-Related Macular Degeneration)—Volume II

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 1513

Special Issue Editors


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Guest Editor
1. Department of Ophthalmology, University of Eastern Finland, Kuopio, Finland
2. Department of Ophthalmology, Kuopio University Hospital, Kuopio, Finland
Interests: autophagy; oxidative stress; inflammation; lysosome; retinal pigment epithelium; reactive oxygen species; lipid peroxidation; age-related macular degeneration
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Guest Editor
Faculty of Health Sciences, School of Pharmacy, University of Eastern Finland, 70210 Kuopio, Finland
Interests: inflammation; allergens; HLA; retinal pigment epithelium; oxidative stress; T lymphocytes; signaling pathways
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Guest Editor
The Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen’s University Belfast, Belfast, UK
Interests: retinal immune regulation; inflammation; aging; retinal degeneration; angiogenesis
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Special Issue Information

Dear Colleagues,

The most common reason for blindness in developed countries is multifactorial age-related macular degeneration (AMD). Its development is associated with aging, gene defects, hypercholesterolemia, hypertension, arteriosclerosis, obesity, smoking, and unhealthy diet. AMD patients experience problems in their daily routines, such as reading, watching TV, driving, and recognizing faces. Straight lines appear wavy or crooked, objects look smaller than normal, and colors are less bright. At the tissue and cellular levels, rod and cone photoreceptors, retinal pigment epithelial cells, and the underlying choroid perform metabolic alterations and degenerative changes in AMD. Chronic oxidative stress, impaired autophagy, mitochondrial dysfunction, and inflammation are strongly linked to AMD.

Reactive oxygen species and oxidized molecules are considered to be major causes of cellular stress, resulting in innate immunity responses through the activation of cell-associated and soluble pattern recognition receptors (PRRs), such as Toll-like or NOD-like receptors (TLR or NLRs), complement factors, scavenger receptors, or pentraxins in AMD pathology. Eventually, chronic oxidative stress, inflammation, and paracellular permeability changes may induce outer blood retinal barrier dysfunction and promote cellular phenotype changes, finally leading to late-stage AMD and visual loss.

A previous Special Issue in Cells, entitled “The Role of Inflammation in AMD (Multifactorial Age-Related Macular Degeneration)”, was very successful. Therefore, we aim to work towards creating an additional Special Issue on this topic.

In this Special Issue, we invite you to provide original clinical reports, experimental studies utilizing cell and animal models, and reviews or shorter perspective articles on all aspects related to the theme of “The Role of Inflammation in AMD”. Expert articles describing genetics/epigenetics, metabolic, mechanistic, functional, cellular, biochemical, or general aspects of inflammation in AMD are welcome.

Prof. Dr. Kai Kaarniranta
Prof. Dr. Anu Kauppinen
Prof. Dr. Heping Xu
Guest Editors

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Keywords

  • aging
  • autophagy
  • degeneration
  • inflammation
  • macula
  • oxidative stress
  • retina

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Published Papers (1 paper)

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Research

15 pages, 2437 KiB  
Article
Metformin Alleviates Inflammation and Induces Mitophagy in Human Retinal Pigment Epithelium Cells Suffering from Mitochondrial Damage
by Maija Toppila, Sofia Ranta-aho, Kai Kaarniranta, Maria Hytti and Anu Kauppinen
Cells 2024, 13(17), 1433; https://doi.org/10.3390/cells13171433 - 27 Aug 2024
Viewed by 1045
Abstract
Mitochondrial malfunction, excessive production of reactive oxygen species (ROS), deficient autophagy/mitophagy, and chronic inflammation are hallmarks of age-related macular degeneration (AMD). Metformin has been shown to activate mitophagy, alleviate inflammation, and lower the odds of developing AMD. Here, we explored the ability of [...] Read more.
Mitochondrial malfunction, excessive production of reactive oxygen species (ROS), deficient autophagy/mitophagy, and chronic inflammation are hallmarks of age-related macular degeneration (AMD). Metformin has been shown to activate mitophagy, alleviate inflammation, and lower the odds of developing AMD. Here, we explored the ability of metformin to activate mitophagy and alleviate inflammation in retinal pigment epithelium (RPE) cells. Human ARPE-19 cells were pre-treated with metformin for 1 h prior to exposure to antimycin A (10 µM), which induced mitochondrial damage. Cell viability, ROS production, and inflammatory cytokine production were measured, while autophagy/mitophagy proteins were studied using Western blotting and immunocytochemistry. Metformin pre-treatment reduced the levels of proinflammatory cytokines IL-6 and IL-8 to 42% and 65% compared to ARPE-19 cells exposed to antimycin A alone. Metformin reduced the accumulation of the autophagy substrate SQSTM1/p62 (43.9%) and the levels of LC3 I and II (51.6% and 48.6%, respectively) after antimycin A exposure. Metformin also increased the colocalization of LC3 with TOM20 1.5-fold, suggesting active mitophagy. Antimycin A exposure increased the production of mitochondrial ROS (226%), which was reduced by the metformin pre-treatment (84.5%). Collectively, metformin showed anti-inflammatory and antioxidative potential with mitophagy induction in human RPE cells suffering from mitochondrial damage. Full article
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