Abstract

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.

Highlights

  • Long non-coding RNAs may be classified in many other ways, and frequently, they are categorized as intergenic long non-coding RNAs (lncRNAs), intronic lncRNAs, bidirectional lncRNAs, overlapping sense lncRNAs, and antisense lncRNAs, lncRNAs hosted by a Micro RNAs (miRNAs) gene or cluster of miRNA genes (Figure 2) [29]

  • The development of bioinformatics resulted in the identification of many lncRNAs that may be important in retinal pathologies, but their functional significance has not been determined in mechanistic studies

  • Several lncRNAs with identified or putative functions may be associated with retinal development and homeostasis, so their impairment may be involved in retinal pathogenesis, including Age-related macular degeneration (AMD)

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Summary

Introduction with regard to jurisdictional claims in

Does everything lie in genes? In a way, yes, as the genetic constitution of an organism determined by the sequence of its genome is a blueprint for an individual, but it represents the only potential for its development in normal conditions. Age-related macular degeneration (AMD) is a common cause of vision loss in the elderly It is a complex, multifactorial eye disease with an interplay between genetic and environmental/lifestyle factors in its pathogenesis. Per definition, the most serious factor of AMD pathogenesis, and several other reported or putative factors may play a role These include modifiable factors, such as tobacco smoking, improper diet, high body-mass index, increased blood lipid, and cholesterol levels, female sex, exposure to the sunlight, especially its blue component, and others (reviewed in the work of [8]). Significant changes in some autophagy markers in the modified animals were not observed in that study, that important work suggests that dedifferentiation of the RPE cells might be induced by oxidative stress and the mTOR signaling, essential in autophagy, can contribute to AMD pathogenesis and can be considered as a potential therapeutic target in this disease. This is likely due to poorer knowledge and higher experimental requirements of lncRNAs as compared with miRNAs

Long Non-Coding RNAs
Long Non-Coding RNAs in AMD
Long Non-Coding RNAs in Retinal Development
Long Non-Coding RNAs in AMD Patients
Long Non-Coding RNAs in AMD Models
Findings
Conclusions and Perspectives
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