Abstract
A consistent association has been observed between leukocyte telomere length (LTL) and atherosclerosis, but the mechanisms underlying these associations are still not well understood. Premature biology aging was evident in atherosclerotic plaques, characterized by reduced cell proliferation, irreversible growth arrest and apoptosis, and telomere attrition. As atherosclerosis is a state of chronic low-grade inflammation and increased oxidative stress, shortened LTL in patients with atherosclerosis might stem from the two sources, one is an accelerated rate in hematopoietic stem cells (HSCs) replication to replace leukocytes consumed in the inflammatory process, and another is the increase in the loss of telomere repeats per replication. Thus, diminished HSC reserves at birth and age-dependent telomere attrition afterward are mirrored in shortened LTL during the adulthood. In addition, the inter-individual variation of LTL in the general population can be partly explained by genetic factors regulating telomere maintenance and the rate of HSCs replication. Atherosclerosis is an aging-related disease, and practically all humans develop atherosclerosis if they live long enough. Here we overview the potential roles of LTL dynamics in the imbalance between injurious oxidative stress/inflammation and endothelial repair during the pathogenesis of age-related atherosclerosis, and discuss the possibility that preventing accelerated cellular senescence is a potential target in prevention of atherosclerosis.
Highlights
Aging, which is broadly defined as the time-dependent functional decline, has attracted curiosity and imagination throughout the history of humankind
As atherosclerosis is a state of chronic low-grade inflammation and increased oxidative stress, shortened leukocyte telomere length (LTL) in patients with atherosclerosis might stem from the two sources, one is an accelerated rate in hematopoietic stem cells (HSCs) replication to replace leukocytes consumed in the inflammatory process, and another is the increase in the loss of telomere repeats per replication
We overview the potential roles of LTL dynamics in the imbalance between injurious oxidative stress/inflammation and endothelial repair during the pathogenesis of age-related atherosclerosis, and discuss the possibility that preventing accelerated cellular senescence is a potential target in prevention of atherosclerosis
Summary
Even in the absence of atherosclerosis, can lead to vascular remodeling characterized by intimal and medial thickening, endothelia cell dysfunction, increased collagen deposition, decreased elastin content, and impaired vessel elasticity, which results in arterial stiffness and related vascular diseases. Replicative senescence occurs with exhaustion of proliferative lifespan over time, and is associated with critically shortened telomeres at chromosome ends. SIPS is not usually characterized by telomere shortening and triggered by external stimuli, such as oxidizing agents and radiation, which activate the intracellular senescence cascade prematurely. Increased numbers of SA G-positive vascular smooth cells (VSMCs), endothelial cells (ECs), and monocyte/macro- phages are observed in aged vessels and atherosclerotic lesions [5,6], reinforcing the idea that atherosclerosis is associated with premature cellular senescence. Recent evidence indicates that peripheral leukocyte telomere length can be used as a systemic marker for cellular senescence and aging-related diseases, which might yield new insights into the underlying molecular mechanisms of vascular aging and improve cardiovascular risk stratification
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