The advancements in science and clinical options has led to the dramatic increase of the age of the population of Western societies. By 2031, 22% of Europeans will be 65 years old or older. This demographic phenomenon creates a new social and medical burden since aging is accompanied by -and may be at least in part the cause of- an increased incidence of cardiovascular diseases (e.g. atherosclerosis, hypertension, myocardial infarction, and heart failure). Endogenous mechanisms of cardiovascular repair and regeneration rely on the functionality of cells (e.g. endothelial cells, pericytes, and various subclasses of circulating leukocytes) that either reside in the cardiovascular system or are recruited from the bone marrow, through circulation.
All of these cellular players are not exempted from the aging-related decline in their functionality that affect the entire organism, and therefore may lose their protective function and in some cases become even deleterious. Indeed during organism aging, cells endowed with reparative potential, as stem/progenitor cells, progressively lose their growth and differentiation capabilities as a result of their exposure to a variety of stressors. The latter, interacting with the genotype of the individuals (that may affect stress resistance), can induce a complex biological response (also known as cell senescence) that, while promoting cell plasticity and tissue repair in acute settings, may induce inflammation and fibrosis in chronic conditions.
Depicting the mechanisms of cardiovascular regenerative cell senescence and what is the role of the potential age-associated changes in the cell ability in maintaining normal tissue homeostasis may help in developing new preventive and therapeutic strategies for cardiovascular diseases.
In this Research Topic we welcome various articles (e.g. reviews, original research or methodology articles) on studies that help in the understanding of and the discussion on the above mentioned age-associated cellular changes.
The advancements in science and clinical options has led to the dramatic increase of the age of the population of Western societies. By 2031, 22% of Europeans will be 65 years old or older. This demographic phenomenon creates a new social and medical burden since aging is accompanied by -and may be at least in part the cause of- an increased incidence of cardiovascular diseases (e.g. atherosclerosis, hypertension, myocardial infarction, and heart failure). Endogenous mechanisms of cardiovascular repair and regeneration rely on the functionality of cells (e.g. endothelial cells, pericytes, and various subclasses of circulating leukocytes) that either reside in the cardiovascular system or are recruited from the bone marrow, through circulation.
All of these cellular players are not exempted from the aging-related decline in their functionality that affect the entire organism, and therefore may lose their protective function and in some cases become even deleterious. Indeed during organism aging, cells endowed with reparative potential, as stem/progenitor cells, progressively lose their growth and differentiation capabilities as a result of their exposure to a variety of stressors. The latter, interacting with the genotype of the individuals (that may affect stress resistance), can induce a complex biological response (also known as cell senescence) that, while promoting cell plasticity and tissue repair in acute settings, may induce inflammation and fibrosis in chronic conditions.
Depicting the mechanisms of cardiovascular regenerative cell senescence and what is the role of the potential age-associated changes in the cell ability in maintaining normal tissue homeostasis may help in developing new preventive and therapeutic strategies for cardiovascular diseases.
In this Research Topic we welcome various articles (e.g. reviews, original research or methodology articles) on studies that help in the understanding of and the discussion on the above mentioned age-associated cellular changes.
