Obesity, type 2 diabetes, and cardiovascular disease (CVD) represent the major global threat for public health and consist of a cluster of immunometabolic disorders, in which aberrant metabolism is linked to activation of immune system components. It is now well recognized that obesity-induced metabolic derangements are strong risk factors for developing atherosclerosis, heart disease and cardiac mortality.
Obesity is characterized by the production of inflammatory cytokines in multiple organs, which leads to local tissue inflammation and further decline in local and systemic insulin sensitivity. Especially adipose tissue has a critical role in the systemic control of insulin sensitivity.
Both basic as well as clinical studies have demonstrated that adipose tissue health is an important denominator of CVD and cardiac mortality. It is now well established that adipose tissue in humans exists in a variety of phenotypes and has high plasticity in response to environmental challenges such as diet, temperature, and physical activity. Throughout the human body, adipose tissues can be found in multiple locations – e.g., visceral, subcutaneous, epicardial adipose tissue, and perivascular depots – all of which are associated with different outcomes on metabolic health. While white adipocytes serve as an important reservoir of lipids and endocrine hormones, thermogenic adipocytes (brown and beige) expresses the unique uncoupling protein 1, which enables these cells to perform thermogenesis, thereby promoting caloric dissipation as heat. In addition to its role in thermogenesis, thermogenic adipose tissue is now well recognized as a highly active metabolic organ involved in the maintenance of systemic metabolic health and possibly cardiac metabolism.
Brown adipose tissue (BAT) dysfunction has been linked to CVD, and activation of BAT has been shown to have cardioprotective roles. However, the underlying mechanisms are yet to be clearly defined both on the molecular levels as well in clinical studies. Particularly interesting is that while obesity is an established risk factor for CVD, patients with existing heart failure have a better prognosis with higher BMI. This is known as “obesity paradox”. It is being speculated that the immunometabolic phenotype of adipose tissue may contribute to this paradoxical relationship. Adipose tissue functions as a metabolic sink, and prevents ectopic lipid deposition in cardiac as well as non-cardiac tissues – i.e., lipotoxicity. For example, there is a clear link of adipose tissue health and nonalcoholic fatty liver disease in patients with heart failure. Nevertheless, their roles, causality, and pathological implications are largely unknown.
This Research Topic is dedicated to articles highlighting our current understanding of:
1) Roles of adipose tissue phenotypes for regulating cardiac as well as systemic metabolism;
2) Impact of adipose tissue phenotypes on CVD in basic and clinical settings;
3) Protective and deleterious roles of adipose-derived cytokines and metabolites in CVD;
4) Medical and surgical therapies targeting adipose tissue loss and/ or phenotypes, and their implications for CVD; and
5) Roles of ectopic lipid deposition in cardiac and non-cardiac tissues in CVD.
This collection of peer-reviewed articles will enhance our understating on the roles of adipose tissues for CVD.
Obesity, type 2 diabetes, and cardiovascular disease (CVD) represent the major global threat for public health and consist of a cluster of immunometabolic disorders, in which aberrant metabolism is linked to activation of immune system components. It is now well recognized that obesity-induced metabolic derangements are strong risk factors for developing atherosclerosis, heart disease and cardiac mortality.
Obesity is characterized by the production of inflammatory cytokines in multiple organs, which leads to local tissue inflammation and further decline in local and systemic insulin sensitivity. Especially adipose tissue has a critical role in the systemic control of insulin sensitivity.
Both basic as well as clinical studies have demonstrated that adipose tissue health is an important denominator of CVD and cardiac mortality. It is now well established that adipose tissue in humans exists in a variety of phenotypes and has high plasticity in response to environmental challenges such as diet, temperature, and physical activity. Throughout the human body, adipose tissues can be found in multiple locations – e.g., visceral, subcutaneous, epicardial adipose tissue, and perivascular depots – all of which are associated with different outcomes on metabolic health. While white adipocytes serve as an important reservoir of lipids and endocrine hormones, thermogenic adipocytes (brown and beige) expresses the unique uncoupling protein 1, which enables these cells to perform thermogenesis, thereby promoting caloric dissipation as heat. In addition to its role in thermogenesis, thermogenic adipose tissue is now well recognized as a highly active metabolic organ involved in the maintenance of systemic metabolic health and possibly cardiac metabolism.
Brown adipose tissue (BAT) dysfunction has been linked to CVD, and activation of BAT has been shown to have cardioprotective roles. However, the underlying mechanisms are yet to be clearly defined both on the molecular levels as well in clinical studies. Particularly interesting is that while obesity is an established risk factor for CVD, patients with existing heart failure have a better prognosis with higher BMI. This is known as “obesity paradox”. It is being speculated that the immunometabolic phenotype of adipose tissue may contribute to this paradoxical relationship. Adipose tissue functions as a metabolic sink, and prevents ectopic lipid deposition in cardiac as well as non-cardiac tissues – i.e., lipotoxicity. For example, there is a clear link of adipose tissue health and nonalcoholic fatty liver disease in patients with heart failure. Nevertheless, their roles, causality, and pathological implications are largely unknown.
This Research Topic is dedicated to articles highlighting our current understanding of:
1) Roles of adipose tissue phenotypes for regulating cardiac as well as systemic metabolism;
2) Impact of adipose tissue phenotypes on CVD in basic and clinical settings;
3) Protective and deleterious roles of adipose-derived cytokines and metabolites in CVD;
4) Medical and surgical therapies targeting adipose tissue loss and/ or phenotypes, and their implications for CVD; and
5) Roles of ectopic lipid deposition in cardiac and non-cardiac tissues in CVD.
This collection of peer-reviewed articles will enhance our understating on the roles of adipose tissues for CVD.