The dramatic increase in the prevalence of diabetes and obesity worldwide has seriously threatened human health since its associated complications cause high morbidity and mortality. Among the complications, cardiovascular diseases are the predominant component. Although various controls for blood glucose and blood pressure are applied, patients with diabetes or obesity and associated metabolic syndromes are still at high risk of developing various cardiovascular diseases, nephropathy, retinopathy, neuropathy, skin disorders, and male infertility. Therefore, we need to understand the mechanisms underlying the pathogenesis of these complications in order to develop more effective therapies to prevent or slow down the progression of diabetic or metabolic syndrome complications.
One of the underlying mechanisms for these cardiovascular diseases is oxidative stress, a critical role in the pathogenesis of diabetic complications. Diabetes-induced overproduction of mitochondrial superoxide leads to a series of detrimental cellular events, including the increased formation of advanced glycation end products (AGEs), increased expression of the receptor for AGEs (RAGE), and activation of protein kinase C isoforms, the polyol pathway, and the hexosamine pathway. These effects consequently result in pathological remodeling of the end-organs and their dysfunction. Hence, targeting diabetes-induced oxidative stress has attracted much research interest in recent years.
Apoptotic cell death has been demonstrated and also considered as one major cell death in the pathogenesis of these cardiovascular complications, however, other kinds of cell deaths have also appreciated playing different important roles either in positive or negative regulation of the cellular and signaling pathways. Therefore, new insights into understanding the roles of various kinds of cell deaths will also be needed.
Even though there is no cure for these cardiovascular diseases related to diabetes and obesity or metabolic syndromes, people with diabetes can prevent or delay the onset of complications by changing their lifestyle and balancing their food intake with exercise. In this Research Topic, we are inviting authors to submit original research papers, as well as review articles, to discuss the current understanding of cellular and molecular pathology, function, signal pathways, and preventive and/or therapeutic insights in diabetic complications.
Potential topics include but are not limited to the following:
• Discovery of oxidative stress-related biomarkers of diabetic complications
• Novel antioxidant therapeutics in diabetic complications
• Genetic and epigenetic mechanisms responsible for the pathogenic signaling pathways in diabetic complications
• Crosstalk between oxidative stress, inflammation, mitochondrial dysfunction, endoplasmic reticulum stress, autophagy, and apoptosis in diabetic complications
• Role of mitochondria in diabetic complications
• New insights into assessment and management of diabetic complications, with an emphasis on oxidative stress and antioxidants
• Molecular triggers, mediators, and regulators of apoptosis, autophagy, ferroptosis, necroptosis, senesces related to diabetes and obesity
• Role of mitochondria-derived reactive oxygen free radicals in the myocardial cell death
• Advances in the development and utility of novel in vitro and pre-clinical experimental models to investigate and understand the pathophysiology of cardiovascular diseases
• Environmental effects on this diabetes- or obesity-related cardiovascular diseases
• Effects of essential and nonessential metals on these cardiovascular diseases
The dramatic increase in the prevalence of diabetes and obesity worldwide has seriously threatened human health since its associated complications cause high morbidity and mortality. Among the complications, cardiovascular diseases are the predominant component. Although various controls for blood glucose and blood pressure are applied, patients with diabetes or obesity and associated metabolic syndromes are still at high risk of developing various cardiovascular diseases, nephropathy, retinopathy, neuropathy, skin disorders, and male infertility. Therefore, we need to understand the mechanisms underlying the pathogenesis of these complications in order to develop more effective therapies to prevent or slow down the progression of diabetic or metabolic syndrome complications.
One of the underlying mechanisms for these cardiovascular diseases is oxidative stress, a critical role in the pathogenesis of diabetic complications. Diabetes-induced overproduction of mitochondrial superoxide leads to a series of detrimental cellular events, including the increased formation of advanced glycation end products (AGEs), increased expression of the receptor for AGEs (RAGE), and activation of protein kinase C isoforms, the polyol pathway, and the hexosamine pathway. These effects consequently result in pathological remodeling of the end-organs and their dysfunction. Hence, targeting diabetes-induced oxidative stress has attracted much research interest in recent years.
Apoptotic cell death has been demonstrated and also considered as one major cell death in the pathogenesis of these cardiovascular complications, however, other kinds of cell deaths have also appreciated playing different important roles either in positive or negative regulation of the cellular and signaling pathways. Therefore, new insights into understanding the roles of various kinds of cell deaths will also be needed.
Even though there is no cure for these cardiovascular diseases related to diabetes and obesity or metabolic syndromes, people with diabetes can prevent or delay the onset of complications by changing their lifestyle and balancing their food intake with exercise. In this Research Topic, we are inviting authors to submit original research papers, as well as review articles, to discuss the current understanding of cellular and molecular pathology, function, signal pathways, and preventive and/or therapeutic insights in diabetic complications.
Potential topics include but are not limited to the following:
• Discovery of oxidative stress-related biomarkers of diabetic complications
• Novel antioxidant therapeutics in diabetic complications
• Genetic and epigenetic mechanisms responsible for the pathogenic signaling pathways in diabetic complications
• Crosstalk between oxidative stress, inflammation, mitochondrial dysfunction, endoplasmic reticulum stress, autophagy, and apoptosis in diabetic complications
• Role of mitochondria in diabetic complications
• New insights into assessment and management of diabetic complications, with an emphasis on oxidative stress and antioxidants
• Molecular triggers, mediators, and regulators of apoptosis, autophagy, ferroptosis, necroptosis, senesces related to diabetes and obesity
• Role of mitochondria-derived reactive oxygen free radicals in the myocardial cell death
• Advances in the development and utility of novel in vitro and pre-clinical experimental models to investigate and understand the pathophysiology of cardiovascular diseases
• Environmental effects on this diabetes- or obesity-related cardiovascular diseases
• Effects of essential and nonessential metals on these cardiovascular diseases
