About this Research Topic
Diabetes mellitus (DM) is increasing dramatically worldwide. 415 million individuals were affected by DM in 2015, and this number is expected to increase to 642 million people in 2040, as estimated by International Diabetes Federation. This poses a severe threat to the world’s public health. DM results in high morbidity and mortality predominantly through vascular complications, such as nephropathy, retinopathy, and DM-driven atherosclerosis-induced ischemic cardiovascular diseases. Notably, diabetic individuals are at high risk of developing vascular complications despite attainment of glycemic control – a phenomenon named “metabolic memory”, leaving a tough problem in the clinical management of DM.
Accumulating evidence has demonstrated a key role for epigenetic modifications without changing DNA sequence, including chromatin histone modifications, DNA methylation, and non-coding RNAs in the pathogenesis of vascular complications of DM (VCDM). Mechanisms or factors such as oxidative stress, inflammation, growth factors, cytokines, super enhancers, bromodomain-containing proteins, mediator complex, as well as others can lead to dysregulation of these epigenetic modifications, contributing to sustained expression of deleterious factors that affect metabolic memory. An understanding of the role of epigenetic mechanisms involved in the pathogenesis of VCDM is clearly warranted as this will not only shed light upon deeper understanding of the pathophysiology of VCDM, but also has the potential for the identification of desirable novel drug targets. The characterization of these epigenetic mechanisms should facilitate the “erasure” of metabolic memory, thereby benefiting the diabetic population.
In this Research Topic, we highlight the emerging role of epigenetics in metabolic memory and VCDM, aiming to exhibit novel discoveries and understanding of this field. Original research and review articles are welcome covering sub-topics including, but not limited to, the following:
• Roles of histone acetylation and deacetylation, as well as their regulatory mechanisms and interventions in VCDM.
• Roles of DNA methylation and demethylation, as well as their regulatory mechanisms and interventions in VCDM.
• Roles of microRNA, circular RNA and long-noncoding RNA, as well as their regulatory mechanisms and interventions in VCDM.
Accumulating evidence has demonstrated a key role for epigenetic modifications without changing DNA sequence, including chromatin histone modifications, DNA methylation, and non-coding RNAs in the pathogenesis of vascular complications of DM (VCDM). Mechanisms or factors such as oxidative stress, inflammation, growth factors, cytokines, super enhancers, bromodomain-containing proteins, mediator complex, as well as others can lead to dysregulation of these epigenetic modifications, contributing to sustained expression of deleterious factors that affect metabolic memory. An understanding of the role of epigenetic mechanisms involved in the pathogenesis of VCDM is clearly warranted as this will not only shed light upon deeper understanding of the pathophysiology of VCDM, but also has the potential for the identification of desirable novel drug targets. The characterization of these epigenetic mechanisms should facilitate the “erasure” of metabolic memory, thereby benefiting the diabetic population.
In this Research Topic, we highlight the emerging role of epigenetics in metabolic memory and VCDM, aiming to exhibit novel discoveries and understanding of this field. Original research and review articles are welcome covering sub-topics including, but not limited to, the following:
• Roles of histone acetylation and deacetylation, as well as their regulatory mechanisms and interventions in VCDM.
• Roles of DNA methylation and demethylation, as well as their regulatory mechanisms and interventions in VCDM.
• Roles of microRNA, circular RNA and long-noncoding RNA, as well as their regulatory mechanisms and interventions in VCDM.
Keywords: VCDM, Diabetes, Metabolic Memory, Epigenetics
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