by A new study published in the journal Aging has shed light on the role of arterial DNA damage in vascular aging. The research, conducted by Samuel I. Bloom, Jordan R. Tucker, Daniel R. Machin, Hossein Abdeahad, AdeLola O. Adeyemo, Tyler G. Thomas, R. Colton Bramwell, Lisa A. Lesniewski, and Anthony J. Donato from The University of Utah, Florida State University, and the Veterans Affairs Medical Center-Salt Lake City, explored the incidence and physiological consequences of DNA damage in arteries, specifically in the microvasculature, in advanced age.
The study focused on the hypothesis that DNA damage within arteries contributes to the impaired arterial function observed in advanced age, which in turn leads to the development of cardiovascular disease (CVD). The researchers began by assessing the abundance of DNA damage in human and mouse lung microvascular endothelial cells and found that aging increases the percentage of cells with DNA damage.
To investigate the physiological consequences of increased arterial DNA damage, the researchers evaluated measures of endothelial function, microvascular and glycocalyx properties, and arterial stiffness in mice lacking or heterozygous for the double-strand DNA break repair protein ATM kinase.
Surprisingly, in young mice, vascular function remained unchanged, leading the researchers to hypothesize that aging is required for the accumulation of DNA damage. Indeed, when compared to wild type littermate controls, aged mice with reduced ATM kinase levels displayed an accelerated vascular aging phenotype. This phenotype was characterized by an increase in arterial DNA damage, signaling of cellular senescence, and impairments in endothelium-dependent dilation due to elevated oxidative stress. Furthermore, these mice showed reduced microvascular density and glycocalyx thickness, as well as increased arterial stiffness.
The findings of this study suggest that DNA damage accumulation in arteries during advanced age contributes to arterial dysfunction, which is a key driver of cardiovascular disease. These results provide insight into the mechanisms underlying vascular aging and highlight the importance of addressing DNA damage in the prevention and treatment of age-related arterial dysfunction and CVD.
The researchers hope that further studies will be conducted to explore potential interventions to mitigate arterial DNA damage and prevent or delay vascular aging. These interventions could potentially include strategies to enhance double-strand DNA break repair or therapeutic approaches aimed at reducing oxidative stress in the arterial environment.
This study contributes to the growing body of research on the role of DNA damage in aging and age-related diseases. Understanding the mechanisms and consequences of DNA damage in the vasculature can inform the development of targeted interventions and therapies to improve cardiovascular health and reduce the burden of disease associated with aging.
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1. Source: Coherent Market Insights, Public sources, Desk research
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