Type 2 diabetic retinopathy (T2DR) is a highly developed manifestation of diabetic retinopathy along with a prominent cause of sightlessness on a global scale. Brain-derived neurotrophic factor (BDNF), which is an associate of neurotrophin family of proteins and enciphered by the BDNF gene is very effectual in shielding retinas from abnormally high blood sugar associated with diabetes in-vitro. Till date, very less number of facts with respect to epigenetic modification is known in T2DR and future aspect associated with epigenetic studies can be explored in this slow progressing disease. Epigenetics have now turned out to be a crucial field of study in bioscience experimentation which regulates gene expression and change their function without any alteration in the DNA sequence in diabetic environment. Histone lysine methylatio take part in alteration of chromatin structure and regulation of gene expression. After going through the available literature, it can be hypothesized that by regulating H3K9 methylation which is a repressive mark, expression level of BDNF can be regulated which in turn can normalize the BDNF-TrkB signaling pathway and may protect apoptosis of human retinal cells in T2DR promoting their survival. mechanizable approach into histone modification may provide the mode for therapeutic function of drugs in T2DR. The present review is focused on histone methylation (H3K9) with respect to BDNF gene expression related to pathogenesis in T2DR and might be helpful for therapeutic purpose.
Type 2 Diabetic Retinopathy (T2DR) associated with major cause of loss of vision throughout world in diabetic individual is the advanced stage of diabetic retinopathy that anguishes retinal blood vessels. Brain derived neurotrophic factor (BDNF) play key role in defending retinas from unusual high concentration of glucose allied with diabetes in vitro by activating high affinity specific receptor tropomyosin-related kinase B (TrkB). Epigenetic modifications usually involve the interaction between genetic and environmental factors leading to development of disease. Histone methyltransferases regulate gene expression by altering chromatin structure through histone lysine methylation. It has been found that G9A act as the biomarker in various types of cancer like lung cancer, cervical cancer thereby down regulating tumour suppressor genes. Moreover, down regulation of BDNF gene has been found to be associated with the overexpression of genes like G9A (EHMT2), GLP in schizophrenia disease which leads to H3K9me2 (Histone 3 Lysine 9) dimethylation, the repressive mark associated with the suppression of gene expression. As per the available literature, it can be hypothesized that inhibition of H3K9 methylation repressive mark with the help of inhibitor might regulate BDNF expression thereby modulating signaling pathway of BDNF which in turn would prevent the damage of retinal cells in Type 2 Diabetic Retinopathy. An in silico approach before performing in vitro experiment is imperative and is helpful. The present study involved the bioinformatics analysis of compounds as an inhibitor of G9A (EHMT2) enzyme. Docking was performed on compounds obtained from NCBI PubChem database using UCSF Chimera, Swissdock, ADME (Absorption, Distribution, Metabolism and Excretion) analysis of compounds was done with the help of SwissADME.
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