Cardiometabolic diseases are driven by both metabolic disorders (obesity, insulin resistance, non-alcoholic fatty liver diseases, and atherosclerosis) and chronic inflammation (e.g. in diabetes, hypertension and autoimmune diseases), leading to coronary artery disease and heart failure.
The perivascular or pericardiac adipose tissue expansion affecting both the systemic and tissue compartment is favored in cardiometabolic disease development. This adipose tissue is a major component of the cardiovascular system that is dysregulated during the consumption of fat-enriched diets. Additionally, fat-enriched diets profoundly impact the response of immune cells in specialized tissues, as well as the activation and differentiation of tissue-resident progenitors. This results in both dysfunction and remodeling that is not limited to tissues, but also to cell activity. The fate of cardiovascular diseases associated with metabolic disorders promotes the imbalance in pro- and anti-inflammatory environments.
Recent advances in this area have shown that epicardial progenitor cells resident in the heart are activated during metabolic disorders that induce adipose tissue expansion and fibrosis remodeling. Furthermore, fatty-rich diets impact the function of cardiomyocytes, notably ionic currents. Despite this, there is still a lack of research in understanding the link between immune responses, resident progenitor cells, and cardiovascular function in metabolic disorders.
Additionally, persistence of systemic and local cardiac inflammation can cause structural and functional impairment of the heart. This could be due to direct damage of the heart muscle, but also by metabolic adaptation induced by the inflammatory signaling. In the setting of cardiometabolic diseases, both cardiomyocytes and immune cells undergo metabolic derangement, including mitochondrial dysfunction, uncoupling of oxidative phosphorylation (OXPHOS) and glycolysis, and shift in substrate utilisation. Since metabolic syndrome has been associated with chronic inflammation as well as cardiac impairment, metabolic derangement might be a key determinant of inflammation-induced cardiometabolic diseases. However, the mechanisms underlying this link warrant further investigation to identify prognostic biomarkers and novel targets for cardioprotection.
Altogether, this Research Topic aims to address the adverse effect of the cellular component of tissues and cardiac metabolic adaption in metabolic inflammation. The goal of this Research Topic is to also increase our understanding of cardiomyopathy diseases to develop new strategies of prevention and therapeutics.
We encourage the submission of Original Research and Review articles that cover the current advances in the role of immunity and inflammation in the mechanisms underlying the alterations of systemic and cellular metabolism, as well as their biological consequences in the context of cardiometabolic diseases.
Cardiometabolic diseases are driven by both metabolic disorders (obesity, insulin resistance, non-alcoholic fatty liver diseases, and atherosclerosis) and chronic inflammation (e.g. in diabetes, hypertension and autoimmune diseases), leading to coronary artery disease and heart failure.
The perivascular or pericardiac adipose tissue expansion affecting both the systemic and tissue compartment is favored in cardiometabolic disease development. This adipose tissue is a major component of the cardiovascular system that is dysregulated during the consumption of fat-enriched diets. Additionally, fat-enriched diets profoundly impact the response of immune cells in specialized tissues, as well as the activation and differentiation of tissue-resident progenitors. This results in both dysfunction and remodeling that is not limited to tissues, but also to cell activity. The fate of cardiovascular diseases associated with metabolic disorders promotes the imbalance in pro- and anti-inflammatory environments.
Recent advances in this area have shown that epicardial progenitor cells resident in the heart are activated during metabolic disorders that induce adipose tissue expansion and fibrosis remodeling. Furthermore, fatty-rich diets impact the function of cardiomyocytes, notably ionic currents. Despite this, there is still a lack of research in understanding the link between immune responses, resident progenitor cells, and cardiovascular function in metabolic disorders.
Additionally, persistence of systemic and local cardiac inflammation can cause structural and functional impairment of the heart. This could be due to direct damage of the heart muscle, but also by metabolic adaptation induced by the inflammatory signaling. In the setting of cardiometabolic diseases, both cardiomyocytes and immune cells undergo metabolic derangement, including mitochondrial dysfunction, uncoupling of oxidative phosphorylation (OXPHOS) and glycolysis, and shift in substrate utilisation. Since metabolic syndrome has been associated with chronic inflammation as well as cardiac impairment, metabolic derangement might be a key determinant of inflammation-induced cardiometabolic diseases. However, the mechanisms underlying this link warrant further investigation to identify prognostic biomarkers and novel targets for cardioprotection.
Altogether, this Research Topic aims to address the adverse effect of the cellular component of tissues and cardiac metabolic adaption in metabolic inflammation. The goal of this Research Topic is to also increase our understanding of cardiomyopathy diseases to develop new strategies of prevention and therapeutics.
We encourage the submission of Original Research and Review articles that cover the current advances in the role of immunity and inflammation in the mechanisms underlying the alterations of systemic and cellular metabolism, as well as their biological consequences in the context of cardiometabolic diseases.
