Aging is one of the major non-reversible risk factors for several chronic diseases, including cardiovascular diseases (CVD), and it is a key cause of multimorbidity, disability, and frailty. The underlying cellular mechanisms are complex and consist of multifactorial processes, such as telomere shortening, systemic low-grade inflammation, oxidative stress, mitochondrial dysfunction, accumulation of senescent cells, and reduced autophagy. CVD is the leading cause of death worldwide, with increasing incidence in aged individuals. Enhanced vascular aging is associated with more severe atherosclerosis and microvascular dysfunction, and it is characterized by pathological vascular remodeling and vascular stiffness.
Inflammation is often observed in aging hearts, with numerous factors promoting cardiac inflammation; circulating pro-inflammatory factors, which are highly elevated in older individuals play a substantial role. Increased levels of circulating pro-inflammatory factors, e.g., CRP and IL-6, are closely associated with cardiovascular pathologies, including myocardial infarction or coronary heart disease. Obesity, hypertension, diabetes, smoking, and atherosclerosis are risk factors in the development of cardiac inflammaging.
Recent research has also emphasized an essential role of biological sex in inflammaging-associated CVD. Loss of estrogen in older females promotes the activation of inflammatory pathways in cardiac aging that are accompanied by a decline in antioxidative defense mechanisms, and mitochondrial biogenesis and function. Furthermore, non-diseased hearts from older women show reduced anti-inflammatory protection, this is reflected by high levels of the pro-inflammatory cytokine IL-12 and low levels of the anti-inflammatory cytokine IL-10. Interestingly, while cardiac inflammation becomes more prominent in aging female hearts, male hearts seem to be less prone to inflammation due to reduced activation of NF-?B during aging. In contrast to non-diseased healthy hearts, NF-?B seems to be directly related to inflammatory processes in male myocardial tissue in age-related diseases such as dilated cardiomyopathy or end-stage myocarditis, as it is strongly upregulated in the diseased hearts solely in males.
The aim of this Research Topic is to highlight the molecular mechanisms, and translational aspects of cardiovascular aging-related inflammation. Areas of research that are of interest to this article collection include cardiac and vascular inflammaging, impaired mitochondrial function in cardiac inflammaging, disturbed autophagy in cardiac inflammaging, fasting and cardiac inflammaging, and exercise and cardiac inflammaging. We welcome the submission of original research, review and opinion articles to this collection that address such topics.
Aging is one of the major non-reversible risk factors for several chronic diseases, including cardiovascular diseases (CVD), and it is a key cause of multimorbidity, disability, and frailty. The underlying cellular mechanisms are complex and consist of multifactorial processes, such as telomere shortening, systemic low-grade inflammation, oxidative stress, mitochondrial dysfunction, accumulation of senescent cells, and reduced autophagy. CVD is the leading cause of death worldwide, with increasing incidence in aged individuals. Enhanced vascular aging is associated with more severe atherosclerosis and microvascular dysfunction, and it is characterized by pathological vascular remodeling and vascular stiffness.
Inflammation is often observed in aging hearts, with numerous factors promoting cardiac inflammation; circulating pro-inflammatory factors, which are highly elevated in older individuals play a substantial role. Increased levels of circulating pro-inflammatory factors, e.g., CRP and IL-6, are closely associated with cardiovascular pathologies, including myocardial infarction or coronary heart disease. Obesity, hypertension, diabetes, smoking, and atherosclerosis are risk factors in the development of cardiac inflammaging.
Recent research has also emphasized an essential role of biological sex in inflammaging-associated CVD. Loss of estrogen in older females promotes the activation of inflammatory pathways in cardiac aging that are accompanied by a decline in antioxidative defense mechanisms, and mitochondrial biogenesis and function. Furthermore, non-diseased hearts from older women show reduced anti-inflammatory protection, this is reflected by high levels of the pro-inflammatory cytokine IL-12 and low levels of the anti-inflammatory cytokine IL-10. Interestingly, while cardiac inflammation becomes more prominent in aging female hearts, male hearts seem to be less prone to inflammation due to reduced activation of NF-?B during aging. In contrast to non-diseased healthy hearts, NF-?B seems to be directly related to inflammatory processes in male myocardial tissue in age-related diseases such as dilated cardiomyopathy or end-stage myocarditis, as it is strongly upregulated in the diseased hearts solely in males.
The aim of this Research Topic is to highlight the molecular mechanisms, and translational aspects of cardiovascular aging-related inflammation. Areas of research that are of interest to this article collection include cardiac and vascular inflammaging, impaired mitochondrial function in cardiac inflammaging, disturbed autophagy in cardiac inflammaging, fasting and cardiac inflammaging, and exercise and cardiac inflammaging. We welcome the submission of original research, review and opinion articles to this collection that address such topics.
