Oxidative stress is a well-known factor responsible for alterations/mutations in DNA. Hyperglycaemia, in conjugation with oxidative stress, significantly exacerbates the genetic implications of oxidative damage to genetic material. In diabetic subjects, Hyperglycaemia -induced oxidative stress sets off a cascade of events leading to genetic modifications. Hyperglycaemia induces ROS through activation of the glycation reaction and electron transport chain in mitochondria. Acute Hyperglycaemia induces downregulation of gene expression in adipose tissue and skeletal muscle along with altered DNA methylation. Elevated levels of ROS and down regulation of ROS scavengers and antioxidant enzymes are associated with various diseases including cancers. Hyperglycaemia is also accountable for abnormal expression of ROS limiting enzymes such SOD1, GPX1, TXNRD1 and TXNRD2. Hyperglycaemia-induced reactive oxygen species increase expression of the receptor for advanced glycation end products (RAGE) and RAGE ligands.
Here we propose to invite studies concerned with genetic modifications associated with elevated ROS and blood glucose levels.
There are various evidences supporting that epigenetic modification, such as DNA methylation, non-coding RNAs, and histone modifications, play a critical role in the molecular mechanism of oxidative stress and hyperglycaemic condition. It has become necessary to deeply evaluate the therapeutical targets that have been suggested and the possible consequences that may occur on the various disease progression. To our knowledge, there are still many open questions that await answers with the epigenetic mechanism in hyperglycemia-induced oxidative stress. Therefore, the goal of this Research Topic is to explore the potential role of oxidative stress-induced epigenetic implications under high glucose levels and uncover the underlying molecular mechanisms and pathways involved in it. It will also cover how hyperglycemia-induced oxidative stress affects epigenetic changes to the chromatin structure via activation of various signaling pathways, regulation of epigenetic factors (DNA methylation, histone modification, chromatin remodeling, and microRNAs), and underlying mechanism involved in various disease states and progression.
Evidence suggests that hyperglycemia can cause epigenetic chromatin changes in target cells by activating signaling pathways that regulate epigenetic factors, resulting in dysregulated expression of vital genes. The persistence of these epigenetic changes may be the mechanism underlying hyperglycemia inducing oxidative stress. Diabetes is a complicated disease, and other factors such as dyslipidemia, nutritional status, and other environmental factors can work together with high glucose to affect the epigenetic state of target cells in damaged tissues via inducing oxidative stress. Furthermore, how these epigenetic alterations are conveyed through numerous cell cycles is also unknown. Since epigenetic mechanisms are usually reversible unlike genetic changes, they represent a window of opportunity for therapeutic intervention. Our proposed work is expected to greatly enhance our understanding of epigenetic states under normal and disease conditions. Published data and explanations will no doubt accelerate the discovery of new therapeutic targets for the treatment of epigenetic-associated complications in relation to glucose metabolism and oxidative stress.
Oxidative stress is a well-known factor responsible for alterations/mutations in DNA. Hyperglycaemia, in conjugation with oxidative stress, significantly exacerbates the genetic implications of oxidative damage to genetic material. In diabetic subjects, Hyperglycaemia -induced oxidative stress sets off a cascade of events leading to genetic modifications. Hyperglycaemia induces ROS through activation of the glycation reaction and electron transport chain in mitochondria. Acute Hyperglycaemia induces downregulation of gene expression in adipose tissue and skeletal muscle along with altered DNA methylation. Elevated levels of ROS and down regulation of ROS scavengers and antioxidant enzymes are associated with various diseases including cancers. Hyperglycaemia is also accountable for abnormal expression of ROS limiting enzymes such SOD1, GPX1, TXNRD1 and TXNRD2. Hyperglycaemia-induced reactive oxygen species increase expression of the receptor for advanced glycation end products (RAGE) and RAGE ligands.
Here we propose to invite studies concerned with genetic modifications associated with elevated ROS and blood glucose levels.
There are various evidences supporting that epigenetic modification, such as DNA methylation, non-coding RNAs, and histone modifications, play a critical role in the molecular mechanism of oxidative stress and hyperglycaemic condition. It has become necessary to deeply evaluate the therapeutical targets that have been suggested and the possible consequences that may occur on the various disease progression. To our knowledge, there are still many open questions that await answers with the epigenetic mechanism in hyperglycemia-induced oxidative stress. Therefore, the goal of this Research Topic is to explore the potential role of oxidative stress-induced epigenetic implications under high glucose levels and uncover the underlying molecular mechanisms and pathways involved in it. It will also cover how hyperglycemia-induced oxidative stress affects epigenetic changes to the chromatin structure via activation of various signaling pathways, regulation of epigenetic factors (DNA methylation, histone modification, chromatin remodeling, and microRNAs), and underlying mechanism involved in various disease states and progression.
Evidence suggests that hyperglycemia can cause epigenetic chromatin changes in target cells by activating signaling pathways that regulate epigenetic factors, resulting in dysregulated expression of vital genes. The persistence of these epigenetic changes may be the mechanism underlying hyperglycemia inducing oxidative stress. Diabetes is a complicated disease, and other factors such as dyslipidemia, nutritional status, and other environmental factors can work together with high glucose to affect the epigenetic state of target cells in damaged tissues via inducing oxidative stress. Furthermore, how these epigenetic alterations are conveyed through numerous cell cycles is also unknown. Since epigenetic mechanisms are usually reversible unlike genetic changes, they represent a window of opportunity for therapeutic intervention. Our proposed work is expected to greatly enhance our understanding of epigenetic states under normal and disease conditions. Published data and explanations will no doubt accelerate the discovery of new therapeutic targets for the treatment of epigenetic-associated complications in relation to glucose metabolism and oxidative stress.
