Abstract
The epigenetic regulation of lncRNA TUG1 has garnered significant attention in the context of diabetes and its associated disorders. TUG1's multifaceted roles in gene expression modulation, and cellular differentiation, and it plays a major role in the growth of diabetes and the issues that are related to it due to pathological processes. In diabetes, aberrant epigenetic modifications can lead to dysregulation of TUG1 expression, contributing to disrupted insulin signaling, impaired glucose metabolism, and beta-cell dysfunction. Moreover, it has been reported that TUG1 contributes to the development of problems linked to diabetes, such as nephropathy, retinopathy, and cardiovascular complications, through epigenetically mediated mechanisms. Understanding the epigenetic regulations of TUG1 offers novel insights into the primary molecular mechanisms of diabetes and provides a possible path for healing interventions. Targeting epigenetic modifications associated with TUG1 holds promise for restoring proper gene expression patterns, ameliorating insulin sensitivity, and mitigating the inception and development of diabetic associative diseases. This review highlights the intricate epigenetic landscape that governs TUG1 expression in diabetes, encompassing DNA methylation and alterations in histone structure, as well as microRNA interactions.