Abstract
Cellular stress, combined with dysfunctional, inadequate mitochondrial phosphorylation, produces an excessive amount of reactive oxygen species (ROS) and an increased level of ROS in cells, which leads to oxidation and subsequent cellular damage. Because of its cell damaging action, an association between anomalous ROS production and disease such as Type 1 (T1D) and Type 2 (T2D) diabetes, as well as their complications, has been well established. However, there is a lack of understanding about genome-driven responses to ROS-mediated cellular stress. Over the last decade, multiple studies have suggested a link between oxidative stress and microRNAs (miRNAs). The miRNAs are small non-coding RNAs that mostly suppress expression of the target gene by interaction with its 3’untranslated region (3′UTR). In this paper, we review the recent progress in the field, focusing on the association between miRNAs and oxidative stress during the progression of diabetes.
Highlights
Diabetes, which affects approximately 422 million people worldwide, is a disease characterized by the loss of glycemic control, which causes side effects such as polyuria, glycosuria, weight loss, neuropathies, retinopathy, and renal plus vascular diseases
Strong evidence indicates that Type 2 diabetes (T2D) is associated with a deficit in beta cell mass [5], which leads to long lasting inefficient glycemic control leading to toxic amount of glucose
We review the progress made in this field, describing mechanistic miRNA-driven gene regulation during oxidative stress and diabetes progression
Summary
Diabetes, which affects approximately 422 million people worldwide, is a disease characterized by the loss of glycemic control, which causes side effects such as polyuria, glycosuria, weight loss, neuropathies, retinopathy, and renal plus vascular diseases. The most prevalent forms of this disease are Type 1 (T1D) and Type 2 diabetes (T2D) Both types are characterized by hyperglycemia due to either insufficient insulin production (T1D) or loss of cellular sensitivity to insulin, known as insulin resistance (T2D). Beta cells are essential for blood glucose homeostasis Their dysregulation is linked to both forms of diabetes. Oxidative stress in T1D originates from T cell-mediated autoimmunity targeting beta cells through the generation of proinflammatory cytokines. Type 2 diabetes is a metabolic syndrome where a group of conditions such as hypertension, glucose intolerance, insulin resistance, obesity, and dyslipidemia result in cellular oxidative stress across tissues [11,12]. Current reports show that changes in miRNA levels contribute to persistent cellular oxidative stress, eventually leading to the development of diseases. We review the progress made in this field, describing mechanistic miRNA-driven gene regulation during oxidative stress and diabetes progression
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