Abstract

Diabetes Mellitus (DM) is one of the major metabolic disorders and its severity leads to death. Enhancement in hyperglycaemic conditions of DM gives rise to endothelial impairment in small and large blood vessels contributing towards microvascular and macrovascular complications respectively. The pathogenesis of diabetic complications is associated with interruption of various signal transduction pathways due to epigenetic modifications such as aberrant histone modifications, DNA methylation and expression of miRNAs along with the long non-coding RNAs (lncRNAs). Amongst these epigenetic alterations, modulated expressions of miRNAs confer to apoptosis and endothelial dysfunction of organs that gives rise to vascular complications. In this review, we principally focussed on physiological role of miR29 family in DM and have discussed crosstalk between miR29 family and numerous genes involved in signal transduction pathways of Diabetic vascular complications. Incidences of diabetic retinopathy exploiting the role of miR29 in regulation of EMT process, differential expression patterns of miR29 and promising therapeutic role of miR29 have been discussed. We have summarised the therapeutic role of miR29 in podocyte impairment and how miR29 regulates the expressions of profibrotic, inflammatory and ECM encoding genes in renal fibrosis under diabetic conditions. We have also highlighted impact of miR29 expression patterns in cardiac angiopathy, cardiomyocyte's apoptosis and cardiac fibrosis. Additionally, we have also presented the contradictory actions of miR29 family in amelioration as well as in enhancement of diabetic complications.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.