This Research Topic is part of the Arrhythmogenic Substrates in Diabetes and Obesity community series:
Community Series in Arrhythmogenic Substrates in Diabetes and Obesity, Volume II Diabetes and obesity are interlinked epidemics contributing to the enhanced risk of arrhythmic events leading to sudden cardiac death. It is known that the pathophysiology of diabetes/obesity involves altered pathways including dyslipidemia, inflammation, fibrosis, hyperglycemia, insulin resistance, and hyperuricemia, which is now collectively referred to as metabolic syndrome. These abnormalities predispose patients to atrial fibrillation, as well as ventricular arrhythmias. Despite this knowledge, the incidence of arrhythmias in diabetic/obese as well metabolic syndrome patients is still on the rise, suggesting the need for novel mechanistic insights from unexplored metabolic signaling pathways. Emerging candidates for modulation in diabetes and obesity includes mitochondrial dysfunction, oxidative stress, autophagy, as well as protein phosphatases (PP2A) and kinases (e.g. 5’-AMP-activated protein kinase = AMPK). In addition to the sensitivity of these signaling pathways to changes in the metabolic state of the cell, they also play a role in regulation of cardiac electrical function through both direct and indirect modulation of the function of major cardiac ionic channels as well as intracellular calcium release channels (RyR).
The objective of this Research Topic is to encourage a series of review papers, perspectives and original articles that summarize or discuss recent advances from clinical and animal studies of cardiomyopathies of diabetes, obesity and metabolic syndrome. Furthermore, in recent years there has been a significant effort to develop more realistic pre-clinical models that using myocytes derived from human stem cells, which are likely to advance our knowledge of the association between metabolic disorders and arrhythmias. Our hope is that this Research Topic will stimulate new ideas and insights and reveal underappreciated Research Topic to the scientific community. This effort is likely to inform development of therapeutic interventions and policy makers on cardiac safety guidelines that will help to improve the lives of patients.
This Research Topic is part of the Arrhythmogenic Substrates in Diabetes and Obesity community series:
Community Series in Arrhythmogenic Substrates in Diabetes and Obesity, Volume II Diabetes and obesity are interlinked epidemics contributing to the enhanced risk of arrhythmic events leading to sudden cardiac death. It is known that the pathophysiology of diabetes/obesity involves altered pathways including dyslipidemia, inflammation, fibrosis, hyperglycemia, insulin resistance, and hyperuricemia, which is now collectively referred to as metabolic syndrome. These abnormalities predispose patients to atrial fibrillation, as well as ventricular arrhythmias. Despite this knowledge, the incidence of arrhythmias in diabetic/obese as well metabolic syndrome patients is still on the rise, suggesting the need for novel mechanistic insights from unexplored metabolic signaling pathways. Emerging candidates for modulation in diabetes and obesity includes mitochondrial dysfunction, oxidative stress, autophagy, as well as protein phosphatases (PP2A) and kinases (e.g. 5’-AMP-activated protein kinase = AMPK). In addition to the sensitivity of these signaling pathways to changes in the metabolic state of the cell, they also play a role in regulation of cardiac electrical function through both direct and indirect modulation of the function of major cardiac ionic channels as well as intracellular calcium release channels (RyR).
The objective of this Research Topic is to encourage a series of review papers, perspectives and original articles that summarize or discuss recent advances from clinical and animal studies of cardiomyopathies of diabetes, obesity and metabolic syndrome. Furthermore, in recent years there has been a significant effort to develop more realistic pre-clinical models that using myocytes derived from human stem cells, which are likely to advance our knowledge of the association between metabolic disorders and arrhythmias. Our hope is that this Research Topic will stimulate new ideas and insights and reveal underappreciated Research Topic to the scientific community. This effort is likely to inform development of therapeutic interventions and policy makers on cardiac safety guidelines that will help to improve the lives of patients.
