Long Noncoding RNAs and Mitochondrial Homeostasis in the Development of Diabetic Retinopathy

Figures

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  Figure 1. Human genome has less than 3% RNAs that can code for proteins, and over 80% of RNAs are noncoding. Depending on the length of their transcripts, noncoding RNAs are classified as ‘small’ and ‘long’ noncoding RNAs. While small noncoding RNAs have less than 200 nucleotides, long noncoding RNAs have over 200 nucleotides.

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  Figure 2. Long noncoding RNAs may have different genomic locations; between two protein coding genes ‘Intergenic’, or located within an intron of a coding gene ‘Intronic’, or overlap with one or more introns and exons of a different transcript on the same or opposite strand, respectively ‘Antisense’, or be within 100 kb of a coding transcript of the opposite strand ‘Bidirectional’, or present in the enhancer regions close to the promoter ‘Enhancer’.

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  Figure 3. Hyperglycemic environment damages mitochondria and also elevates levels of various nuclear genome encoded LncRNAs including LncMALAT1 and LncNEAT1. These LncRNAs, in addition to affecting metabolic abnormalities associated with diabetic retinopathy including inflammation, also move inside the mitochondria, and damage mitochondrial structural, functional and genomic stability. Furthermore, possible decrease in the mitochondrial genome encoded LncCytB further damages the mitochondria, and the damaged mitochondria accelerates apoptosis, ultimately, resulting in the development of diabetic retinopathy.