Life expectancy is steadily increasing worldwide, inevitably leading to an aging population. Among age-related conditions that negatively influence longevity, vascular aging plays a central role. Indeed, the aged vascular wall presents an enhanced pro-inflammatory environment, which is characterized by an up-regulation of pro-inflammatory molecules and by a down-regulation of their anti-inflammatory counterparts. Within individual vascular cells, pro-inflammatory signaling pathways that control the expression and function of proteins, mRNA and micro RNA (miRNA), are up-regulated in both endothelial and vascular smooth muscle cells.
With advancing age, abnormal integration of the signaling pathways that control the above-mentioned molecular scenario, drives an increase in necrosis, apoptosis and senescence of the endothelial cells, and a decrease in regenerative capacity. This facilitates an increase in the proliferation, migration, invasion, senescence and apoptosis of vascular smooth muscle cells. Additionally, age-related phenotypic changes of vascular cells are accompanied by an increase in the accumulation, deposition, and modification of the extracellular matrix, leading to a pathological vascular restructuring.
The interactions among vascular cells, and with an aged microenvironment, produce a fertile pro-inflammatory soil which is known as “age associated arterial secretory phenotype” (AAASP). This facilitates the onset and progression of vascular diseases – such as hypertension, atherosclerosis, and stroke – via an enhancement of the susceptibility to a pathologic insult or a decrease of the main culprit threshold levels.
Importantly, the heart is a part of the specialized vascular system. Indeed, vascular aging is coupled with myocardial and brain aging, hence contributing to “coupling or decoupling diseases” such as heart failure, impairment of cognition and even dementia such as the Alzheimer’s disease. In this light, targeting the AAASP may be new potential therapeutic strategy.
With this Research Topic, we aim to supply an updated overview of both physiological and biochemical mechanisms that impact vascular aging in a negative or positive way. Also, this topic would like to focus on the signaling mechanisms that orchestrates the important cross talk between vascular aging, heart and brain related diseases. We believe that this topic will contribute to the understanding of the pathogenesis of many chronic or age-related diseases, as well as to their treatment with both current and new therapeutic approaches.
Investigators can contribute original research articles and review articles as well as clinical studies that will stimulate the continuing efforts to understand the etiologies, pathogenesis, diagnosis, treatment and prevention of arterial aging, and age-associated arterial diseases.
Life expectancy is steadily increasing worldwide, inevitably leading to an aging population. Among age-related conditions that negatively influence longevity, vascular aging plays a central role. Indeed, the aged vascular wall presents an enhanced pro-inflammatory environment, which is characterized by an up-regulation of pro-inflammatory molecules and by a down-regulation of their anti-inflammatory counterparts. Within individual vascular cells, pro-inflammatory signaling pathways that control the expression and function of proteins, mRNA and micro RNA (miRNA), are up-regulated in both endothelial and vascular smooth muscle cells.
With advancing age, abnormal integration of the signaling pathways that control the above-mentioned molecular scenario, drives an increase in necrosis, apoptosis and senescence of the endothelial cells, and a decrease in regenerative capacity. This facilitates an increase in the proliferation, migration, invasion, senescence and apoptosis of vascular smooth muscle cells. Additionally, age-related phenotypic changes of vascular cells are accompanied by an increase in the accumulation, deposition, and modification of the extracellular matrix, leading to a pathological vascular restructuring.
The interactions among vascular cells, and with an aged microenvironment, produce a fertile pro-inflammatory soil which is known as “age associated arterial secretory phenotype” (AAASP). This facilitates the onset and progression of vascular diseases – such as hypertension, atherosclerosis, and stroke – via an enhancement of the susceptibility to a pathologic insult or a decrease of the main culprit threshold levels.
Importantly, the heart is a part of the specialized vascular system. Indeed, vascular aging is coupled with myocardial and brain aging, hence contributing to “coupling or decoupling diseases” such as heart failure, impairment of cognition and even dementia such as the Alzheimer’s disease. In this light, targeting the AAASP may be new potential therapeutic strategy.
With this Research Topic, we aim to supply an updated overview of both physiological and biochemical mechanisms that impact vascular aging in a negative or positive way. Also, this topic would like to focus on the signaling mechanisms that orchestrates the important cross talk between vascular aging, heart and brain related diseases. We believe that this topic will contribute to the understanding of the pathogenesis of many chronic or age-related diseases, as well as to their treatment with both current and new therapeutic approaches.
Investigators can contribute original research articles and review articles as well as clinical studies that will stimulate the continuing efforts to understand the etiologies, pathogenesis, diagnosis, treatment and prevention of arterial aging, and age-associated arterial diseases.
