Abstract
Aging is a natural process that affects all systems of the human organism, leading to its inability to adapt to environmental changes. Advancing age has been correlated with various pathological conditions, especially cardiovascular and cerebrovascular diseases. Carotid artery (CA) is mainly affected by age-induced functional and morphological alterations causing atheromatous disease. The evolvement of biomedical sciences has allowed the elucidation of many aspects of this condition. Symptomatic carotid disease (CD) derives from critical luminar stenosis or eruption of an atheromatous plaque due to structural modifications of the vessels, such as carotid intima-media thickening. At a histologic level, the aforementioned changes are mediated by elastin fragmentation, collagen deposition, immune cell infiltration, and accumulation of cytokines and vasoconstrictors. Underlying mechanisms include chronic inflammation and oxidative stress, dysregulation of cellular homeostatic systems, and senescence. Thus, there is an imbalance in components of the vessel wall, which fails to counteract exterior stress stimuli. Consequently, arterial relaxation is impaired and atherosclerotic lesions progress. This is a review of current evidence regarding the relationship of aging with vascular senescence and CD. A deeper understanding of these mechanisms can contribute to the production of efficient prevention methods and targeted therapeutic strategies.
Highlights
Carotid disease (CD) is one of the most common age-related diseases. It refers to a number of macroscopic morphological changes and to alterations at cytopathological level in common carotid artery (CCA) and internal carotid artery (ICA) that lead to cerebrovascular events such as strokes and transient ischemic attacks (TIAs) that comprise a major cause of mortality and morbidity, especially amongst the elderly [1]
Vascular senescence refers to the establishment of clinical and subclinical structural and functional changes at a histological and cellular level, involving cells and the extracellular matrix of vessel walls [3] that are related with the loss of its homeostatic potential to adapt to environmental stress stimuli
Native low-density lipoprotein (LDL) molecules are inactive, oxidative stress involved in atherosclerosis process, turns them into the highly immunogenic oxidized LDLs (oxLDLs), which trigger the production of endothelial adhesion molecules, attract monocytes, and enhance proinflammatory gene activity [16, 27, 74]
Summary
Carotid disease (CD) is one of the most common age-related diseases. It refers to a number of macroscopic morphological changes and to alterations at cytopathological level in common carotid artery (CCA) and internal carotid artery (ICA) that lead to cerebrovascular events such as strokes and transient ischemic attacks (TIAs) that comprise a major cause of mortality and morbidity, especially amongst the elderly [1]. Vascular senescence refers to the establishment of clinical and subclinical structural and functional changes at a histological and cellular level, involving cells and the extracellular matrix of vessel walls [3] that are related with the loss of its homeostatic potential to adapt to environmental stress stimuli It is a separate entity from aging, provoked by ageing itself, and by the aforementioned atherogenic factors [2]. Aging is a natural process that causes multiple changes to the human organism decreasing its ability to maintain its homeostasis and make it more vulnerable to threats It is associated with the impairment of vascular function and onset of cardiovascular disease [5, 6] even in the absence of other risk factors [7, 8]. The age-associated plaque morphology seems to change towards more vulnerable plaques, [25, 28] the rupture of which leads to acute cerebrovascular and cardiovascular events, which increase in incidence with age
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