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: 31 October 2024 | Viewed by 300

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

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


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

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