| Autor: |
Blasiak J; Department of Molecular Genetics, Faculty of Biology and Environmental Protection, University of Lodz, Pomorska 141/143, 90-236 Lodz, Poland., Hyttinen JMT; Department of Ophthalmology, University of Eastern Finland, 70210 Kuopio, Finland., Szczepanska J; Department of Pediatric Dentistry, Medical University of Lodz, 92-216 Lodz, Poland., Pawlowska E; Department of Orthodontics, Medical University of Lodz, 92-217 Lodz, Poland., Kaarniranta K; Department of Ophthalmology, University of Eastern Finland, 70210 Kuopio, Finland.; Department of Ophthalmology, Kuopio University Hospital, 70210 Kuopio, Finland. |
| Abstrakt: |
Age-related macular degeneration (AMD) is the leading cause of visual impairment in the aging population with poorly known pathogenesis and lack of effective treatment. Age and family history are the strongest AMD risk factors, and several loci were identified to contribute to AMD. Recently, also the epigenetic profile was associated with AMD, and some long non-coding RNAs (lncRNAs) were shown to involve in AMD pathogenesis. The Vax2os1/2 (ventral anterior homeobox 2 opposite strand isoform 1) lncRNAs may modulate the balance between pro- and anti-angiogenic factors in the eye contributing to wet AMD. The stress-induced dedifferentiation of retinal pigment epithelium cells can be inhibited by the ZNF503-AS1 (zinc finger protein 503 antisense RNA 2) and LINC00167 lncRNAs. Overexpression of the PWRN2 (Prader-Willi region non-protein-coding RNA 2) lncRNA aggravated RPE cells apoptosis and mitochondrial impairment induced by oxidative stress. Several other lncRNAs were reported to exert protective or detrimental effects in AMD. However, many studies are limited to an association between lncRNA and AMD in patients or model systems with bioinformatics. Therefore, further works on lncRNAs in AMD are rational, and they should be enriched with mechanistic and clinical studies to validate conclusions obtained in high-throughput in vitro research. |
