Metabolic syndrome is a condition that involves disruption of energy homeostasis in several organs and tissues, such as adipose tissue, liver, and pancreas including the immune system. Autophagy has emerged as a key player in metabolic disturbances, involved in adipocyte differentiation and adipogenesis, enhancing fat accumulation in the fat depots, with the potential of playing an important role in ß-cell physiology and function, thereby influencing the regulation of the delicate balance between insulin and glucagon. By unraveling the mechanisms underlying the crosstalk between immune inflammatory cells (e.g. macrophages, neutrophils, T and B lymphocytes) and autophagy, we will move towards early diagnosis and improved treatments for patients with metabolic syndrome.
Among the characteristics of metabolic syndrome, dyslipidemia and hypertension seem to be the most important players. Obesity is a chronic metabolic disease that may be associated with other pathological disorders, such as type 2 diabetes mellitus. Studies have shown common pathways linking obesity (as well as overweight) and diabetes (both types 1 and 2) to insulin. In obesity, tissue macrophages and the pro-inflammatory cytokine profile in adipose tissue, might promote glucose intolerance and insulin signaling. In obesity, tissue macrophages and pro-inflammatory cytokine profile in adipose tissue affect glucose intolerance and insulin resistance. Recent studies have linked autophagy disruption and metabolic syndrome burden. It is also believed that dysregulated autophagy is linked to type 1 and 2 diabetes by triggering the development of inflammation and insulin resistance. Understanding the molecular mechanisms involved in the crosstalk between autophagy and metabolic syndrome can bring direct benefits to the patients, improving their quality of life.
In this Research Topic, we welcome Review and Original Research articles that shed light on our understanding of mechanisms by which hormones can influence inflammatory and/or autophagy processes, and how this leads to cardiovascular and metabolic disorders. In particular, we focus on the following points:
• Link between inflammation, autophagy, metabolic and chronic disorders, including obesity, type 1 and 2 diabetes, cardiovascular disease.
• The role of hormones in immune inflammatory cells (e.g. macrophages, neutrophils, T and B lymphocytes) and the consequent dysregulation of metabolic pathways that may contribute to the development of metabolic syndrome.
• How adipose tissue plays a pivotal role in energy metabolism and influences the burden of inflammatory phenotype.
• Cellular processes related to metabolic syndrome including autophagy.
• Components that may contribute for metabolic syndrome burden such as renin angiotensin system, hypertension and dyslipidemia.
Metabolic syndrome is a condition that involves disruption of energy homeostasis in several organs and tissues, such as adipose tissue, liver, and pancreas including the immune system. Autophagy has emerged as a key player in metabolic disturbances, involved in adipocyte differentiation and adipogenesis, enhancing fat accumulation in the fat depots, with the potential of playing an important role in ß-cell physiology and function, thereby influencing the regulation of the delicate balance between insulin and glucagon. By unraveling the mechanisms underlying the crosstalk between immune inflammatory cells (e.g. macrophages, neutrophils, T and B lymphocytes) and autophagy, we will move towards early diagnosis and improved treatments for patients with metabolic syndrome.
Among the characteristics of metabolic syndrome, dyslipidemia and hypertension seem to be the most important players. Obesity is a chronic metabolic disease that may be associated with other pathological disorders, such as type 2 diabetes mellitus. Studies have shown common pathways linking obesity (as well as overweight) and diabetes (both types 1 and 2) to insulin. In obesity, tissue macrophages and the pro-inflammatory cytokine profile in adipose tissue, might promote glucose intolerance and insulin signaling. In obesity, tissue macrophages and pro-inflammatory cytokine profile in adipose tissue affect glucose intolerance and insulin resistance. Recent studies have linked autophagy disruption and metabolic syndrome burden. It is also believed that dysregulated autophagy is linked to type 1 and 2 diabetes by triggering the development of inflammation and insulin resistance. Understanding the molecular mechanisms involved in the crosstalk between autophagy and metabolic syndrome can bring direct benefits to the patients, improving their quality of life.
In this Research Topic, we welcome Review and Original Research articles that shed light on our understanding of mechanisms by which hormones can influence inflammatory and/or autophagy processes, and how this leads to cardiovascular and metabolic disorders. In particular, we focus on the following points:
• Link between inflammation, autophagy, metabolic and chronic disorders, including obesity, type 1 and 2 diabetes, cardiovascular disease.
• The role of hormones in immune inflammatory cells (e.g. macrophages, neutrophils, T and B lymphocytes) and the consequent dysregulation of metabolic pathways that may contribute to the development of metabolic syndrome.
• How adipose tissue plays a pivotal role in energy metabolism and influences the burden of inflammatory phenotype.
• Cellular processes related to metabolic syndrome including autophagy.
• Components that may contribute for metabolic syndrome burden such as renin angiotensin system, hypertension and dyslipidemia.
