Non-Coding RNAs Regulating Mitochondrial Functions and the Oxidative Stress Response as Putative Targets against Age-Related Macular Degeneration (AMD).
Juha M T HyttinenJanusz BlasiakKai KaarnirantaPublished in: International journal of molecular sciences (2023)
Age-related macular degeneration (AMD) is an ever-increasing, insidious disease which reduces the quality of life of millions of elderly people around the world. AMD is characterised by damage to the retinal pigment epithelium (RPE) in the macula region of the retina. The origins of this multi-factorial disease are complex and still not fully understood. Oxidative stress and mitochondrial imbalance in the RPE are believed to be important factors in the development of AMD. In this review, the regulation of the mitochondrial function and antioxidant stress response by non-coding RNAs (ncRNAs), newly emerged epigenetic factors, is discussed. These molecules include microRNAs, long non-coding RNAs, and circular non-coding RNAs. They act mainly as mRNA suppressors, controllers of other ncRNAs, or by interacting with proteins. We include here examples of these RNA molecules which affect various mitochondrial processes and antioxidant signaling of the cell. As a future prospect, the possibility to manipulate these ncRNAs to strengthen mitochondrial and antioxidant response functions is discussed. Non-coding RNAs could be used as potential diagnostic markers for AMD, and in the future, also as therapeutic targets, either by suppressing or increasing their expression. In addition to AMD, it is possible that non-coding RNAs could be regulators in other oxidative stress-related degenerative diseases.
Keyphrases
- age related macular degeneration
- oxidative stress
- long non coding rna
- diabetic rats
- ischemia reperfusion injury
- dna damage
- induced apoptosis
- poor prognosis
- current status
- dna methylation
- gene expression
- binding protein
- risk assessment
- heat shock
- transcription factor
- diabetic retinopathy
- stem cells
- mesenchymal stem cells
- cell therapy
- heat stress
- signaling pathway
- protein kinase
- bone marrow