Metabolic syndrome (MetS) forms a cluster of metabolic dysregulations, including abdominal obesity, atherogenic dyslipidemia, hypertension, hyperglycemia and insulin resistance. It is a prothrombotic and proinflammatory state characterized by increased activity of inflammatory cytokines. The aging of the world population is a major contributor to the growing prevalence of metabolic syndrome, as older adults tend to be affected by the cardiovascular and metabolic risk factors that constitute the syndrome.
Pyroptosis is a type of cell death that ultimately leads to the loss of plasma membrane integrity and is caused by the activation of inflammasome sensors. These include the Nod-like receptor (NLR) family, the DNA receptor Absent in Melanoma 2 (AIM2), and the Pyrin receptor. Pyroptosis plays a critical role in a variety of human diseases, including atherosclerosis, obesity, diabetes, and Alzheimer's disease, which usually release pyroptosis-related cytokines, often due to inflammation.
The increased risk for type 2 diabetes and cardiovascular disease requires treatment for those at high risk, and the fundamental approach is weight reduction and increased physical activity. Regular exercise reduces the risk of chronic metabolic and cardiorespiratory diseases, partially because of its anti-inflammatory effects. Studies have also shown that aerobic exercise is a good option for reducing the release of pyroptosis-related cytokines.
This Research Topic aims to investigate how exercise improves metabolic syndrome by inhibiting pyroptosis. The anti-inflammatory effects of regular exercise may be mediated by a reduction in visceral fat mass that releases adipokines and the anti-inflammatory environment induced by each bout of exercise. In addition, exercise-induced changes in exerkine concentration may be relevant to the metabolic control of patients with type 2 diabetes mellitus and could serve as potential therapeutic targets for atherosclerosis. However, the effect of exercise on pyroptosis in metabolic syndrome and the underlying mechanism is unclear. Studies could discuss the mechanism of the effect of exercise on inflammatory state and pyroptosis in metabolic syndrome, as well as how exercise (both acute and chronic) exerts its anti-inflammatory and anti-pyroptosis effects.
We welcome submissions of Original Research and Review articles in the following scope, but not limited to the following topics:
• How exercise attenuates the inflammatory state of diabetes by inhibiting pyroptosis;
• How exercise prevents chronic inflammatory state in obese or overweight individuals by alleviating pyroptosis;
• How exercise improves the inflammatory state of metabolic syndrome by reducing pyroptosis;
• How exercise promotes the secretion of exerkines by skeletal muscle to regulate the inflammatory state.
Metabolic syndrome (MetS) forms a cluster of metabolic dysregulations, including abdominal obesity, atherogenic dyslipidemia, hypertension, hyperglycemia and insulin resistance. It is a prothrombotic and proinflammatory state characterized by increased activity of inflammatory cytokines. The aging of the world population is a major contributor to the growing prevalence of metabolic syndrome, as older adults tend to be affected by the cardiovascular and metabolic risk factors that constitute the syndrome.
Pyroptosis is a type of cell death that ultimately leads to the loss of plasma membrane integrity and is caused by the activation of inflammasome sensors. These include the Nod-like receptor (NLR) family, the DNA receptor Absent in Melanoma 2 (AIM2), and the Pyrin receptor. Pyroptosis plays a critical role in a variety of human diseases, including atherosclerosis, obesity, diabetes, and Alzheimer's disease, which usually release pyroptosis-related cytokines, often due to inflammation.
The increased risk for type 2 diabetes and cardiovascular disease requires treatment for those at high risk, and the fundamental approach is weight reduction and increased physical activity. Regular exercise reduces the risk of chronic metabolic and cardiorespiratory diseases, partially because of its anti-inflammatory effects. Studies have also shown that aerobic exercise is a good option for reducing the release of pyroptosis-related cytokines.
This Research Topic aims to investigate how exercise improves metabolic syndrome by inhibiting pyroptosis. The anti-inflammatory effects of regular exercise may be mediated by a reduction in visceral fat mass that releases adipokines and the anti-inflammatory environment induced by each bout of exercise. In addition, exercise-induced changes in exerkine concentration may be relevant to the metabolic control of patients with type 2 diabetes mellitus and could serve as potential therapeutic targets for atherosclerosis. However, the effect of exercise on pyroptosis in metabolic syndrome and the underlying mechanism is unclear. Studies could discuss the mechanism of the effect of exercise on inflammatory state and pyroptosis in metabolic syndrome, as well as how exercise (both acute and chronic) exerts its anti-inflammatory and anti-pyroptosis effects.
We welcome submissions of Original Research and Review articles in the following scope, but not limited to the following topics:
• How exercise attenuates the inflammatory state of diabetes by inhibiting pyroptosis;
• How exercise prevents chronic inflammatory state in obese or overweight individuals by alleviating pyroptosis;
• How exercise improves the inflammatory state of metabolic syndrome by reducing pyroptosis;
• How exercise promotes the secretion of exerkines by skeletal muscle to regulate the inflammatory state.
