MicroRNAs Mediated Regulation of Brain Derived Neurotrophic Factor Expression in Type 2 Diabetes Retinopathy

Abstract

Type 2 Diabetic Retinopathy (T2DR) is one of the most common impediments of diabetes that affect the blood vessels of the retina, leading to loss of vision. At the advance proliferative stage of diabetic retinopathy, retina triggers the abnormal angiogenesis, which is instigated due to the increased expression of growth factors such as vascular endothelial growth factor (VEGF), Insulin-like growth factor (IGF-1). Existing therapies are solely directed towards advanced T2DR stages often following permanent damage and are therefore highly anticipated for treatments that are preventive or address early pathology. It is suggested that apoptosis is experienced at the early stages of T2DR in specific retinal ganglions and retinal neurodegeneration probably involves an inadequate level of BDNF. Neuroprotection therapeutic strategies, including somatostatin, brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are more substantial. BDNF, a Neurotrophic factor derived from brain, also known as ANON2, BULN2 is a neurotrophin, and previous studies have reported decreases in BDNF levels in diabetic retina, causing damage to neurons, resulting in neurodegeneration due to its abuse of retinal neurons through the TrkB / ERK / MAPK pathway. MicroRNA (miRNAs) is a class of small, endogenous transcripts of RNA shaped like hairpin with a length of 21 to 25 nucleotides. As stated in the literature, miRNAs bind their target mRNAs to the 5′ end through a completely complementary seed of 7-8 nucleotides and a less complementary area at the 3′ end, which leads to translational repression or mRNA degradation. Finally, this review will helps us to better understand molecular mechanisms through which miRNAs may be viewed as diagnostic or predictive biomarkers and, most importantly, therapeutic targets.