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lncRNA - Long Non-coding RNAs

lncRNA - Long Non-coding RNAs

In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...

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Mitochondrial Fragmentation and Long Noncoding RNA MALAT1 in Diabetic Retinopathy.

Renu A Kowluru¹, Jay Kumar¹

¹Ophthalmology, Visual and Anatomical Sciences, Kresge Eye Institute, Wayne State University, Detroit, MI 48201, USA.

International Journal of Molecular Sciences

|July 12, 2025

Summary

High glucose in diabetic retinopathy upregulates MALAT1, causing Mfn2 gene hypermethylation and mitochondrial damage. Inhibiting MALAT1 protects mitochondria and may prevent diabetic blindness.

Keywords:

DNA methylation MALAT1 diabetic retinopathy long noncoding RNA mitochondria

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Area of Science:

Mitochondrial dynamics
Epigenetics
Diabetic retinopathy

Background:

Mitochondrial fusion-fission is crucial for cellular energy and impaired in diabetic retinopathy.
The fusion gene Mfn2 shows hypermethylated promoter DNA and reduced expression in this condition.
Long noncoding RNAs (LncRNAs) like MALAT1 are implicated in diabetes-related inflammation and gene expression.

Purpose of the Study:

To investigate the role of MALAT1 in mitochondrial dynamics within diabetic retinopathy.
To determine if MALAT1 influences Mfn2 expression and mitochondrial integrity under high glucose conditions.

Main Methods:

Human retinal endothelial cells (HRECs) and Muller cells (RMCs) were transfected with MALAT1-siRNA and exposed to high glucose.
Mfn2 expression, activity, and promoter DNA methylation were quantified.
Mitochondrial integrity was assessed via fragmentation, ultrastructure, membrane potential, and oxygen consumption.

Main Results:

High glucose upregulated MALAT1 and downregulated Mfn2 expression and activity in HRECs and RMCs.
MALAT1-siRNA transfection reversed high glucose-induced Mfn2 promoter hypermethylation and restored Mfn2 activity.
MALAT1-siRNA protected cells against mitochondrial fragmentation, structural damage, and reduced oxygen consumption.

Conclusions:

Upregulated MALAT1 in diabetes promotes Mfn2 promoter hypermethylation in retinal cells, suppressing Mfn2 and damaging mitochondria.
Targeting MALAT1 offers a potential therapeutic strategy to protect mitochondria and prevent vision loss in diabetic retinopathy.