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Relationship Between Biochemical Pathways and Non-Coding RNAs Involved in the Progression of Diabetic Retinopathy

Overview
Journal J Clin Med
Specialty General Medicine
Date 2024 Jan 11
PMID 38202299
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Abstract

Diabetic retinopathy (DR) is a progressive blinding disease, which affects the vision and quality of life of patients, and it severely impacts the society. This complication, caused by abnormal glucose metabolism, leads to structural, functional, molecular, and biochemical abnormalities in the retina. Oxidative stress and inflammation also play pivotal roles in the pathogenic process of DR, leading to mitochondrial damage and a decrease in mitochondrial function. DR causes retinal degeneration in glial and neural cells, while the disappearance of pericytes in retinal blood vessels leads to alterations in vascular regulation and stability. Clinical changes include dilatation and blood flow changes in response to the decrease in retinal perfusion in retinal blood vessels, leading to vascular leakage, neovascularization, and neurodegeneration. The loss of vascular cells in the retina results in capillary occlusion and ischemia. Thus, DR is a highly complex disease with various biological factors, which contribute to its pathogenesis. The interplay between biochemical pathways and non-coding RNAs (ncRNAs) is essential for understanding the development and progression of DR. Abnormal expression of ncRNAs has been confirmed to promote the development of DR, suggesting that ncRNAs such as miRNAs, lncRNAs, and circRNAs have potential as diagnostic biomarkers and theranostic targets in DR. This review provides an overview of the interactions between abnormal biochemical pathways and dysregulated expression of ncRNAs under the influence of hyperglycemic environment in DR.

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References
1.
Aprea J, Prenninger S, Dori M, Ghosh T, Monasor L, Wessendorf E . Transcriptome sequencing during mouse brain development identifies long non-coding RNAs functionally involved in neurogenic commitment. EMBO J. 2013; 32(24):3145-60. PMC: 3981144. DOI: 10.1038/emboj.2013.245. View

2.
Curtis T, Gardiner T, Stitt A . Microvascular lesions of diabetic retinopathy: clues towards understanding pathogenesis?. Eye (Lond). 2009; 23(7):1496-508. DOI: 10.1038/eye.2009.108. View

3.
Chilelli N, Burlina S, Lapolla A . AGEs, rather than hyperglycemia, are responsible for microvascular complications in diabetes: a "glycoxidation-centric" point of view. Nutr Metab Cardiovasc Dis. 2013; 23(10):913-9. DOI: 10.1016/j.numecd.2013.04.004. View

4.
Madsen-Bouterse S, Zhong Q, Mohammad G, Ho Y, Kowluru R . Oxidative damage of mitochondrial DNA in diabetes and its protection by manganese superoxide dismutase. Free Radic Res. 2010; 44(3):313-21. PMC: 3025400. DOI: 10.3109/10715760903494168. View

5.
Bianco L, Arrigo A, Aragona E, Antropoli A, Berni A, Saladino A . Neuroinflammation and neurodegeneration in diabetic retinopathy. Front Aging Neurosci. 2022; 14:937999. PMC: 9424735. DOI: 10.3389/fnagi.2022.937999. View