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The Aging Risk and Atherosclerosis: A Fresh Look at Arterial Homeostasis
Trajen Head1, Sylvia Daunert1, Pascal J Goldschmidt-Clermont2
1Department of Biochemistry and Molecular Biology, University of Miami Miller School of Medicine, Miami, FL, United States.
Insights
Aging significantly accelerates atherosclerosis, leading to cardiovascular disease (CVD) complications. This review explores how aging impacts arterial health, focusing on cellular senescence and immune cell roles in plaque development.
Area of Science:
- Cardiovascular Science
- Aging Research
- Immunology
Background:
- Atherosclerosis is a primary cause of cardiovascular disease (CVD).
- Aging is the most significant risk factor for atherosclerotic lesion development.
- Traditional CVD risk factors do not fully explain the impact of aging on atherosclerosis.
Purpose of the Study:
- To review the pathological and biochemical mechanisms of atherosclerotic plaque formation and progression.
- To investigate the specific impact of aging on arterial homeostasis.
- To highlight recent advances in understanding aging-driven atherosclerosis.
Main Methods:
- Literature review of pathological and biochemical processes in atherosclerosis.
- Focus on aging's influence on arterial homeostasis.
- Examination of bone marrow-derived vascular progenitor cells, monocyte subpopulations, and cellular senescence.
Main Results:
- Aging exacerbates atherosclerotic plaque formation beyond traditional risk factors.
- Cellular senescence and specific immune cell dynamics are key contributors to aging-related atherosclerosis.
- Recent research offers new insights into the mechanisms driving this disease.
Conclusions:
- Aging profoundly influences atherosclerosis through mechanisms independent of traditional risk factors.
- Understanding cellular senescence and immune cell roles is crucial for addressing aging-driven CVD.
- Further research into these aging-specific pathways can lead to novel therapeutic strategies.
Abstract:
A considerable volume of research over the last decade has focused on understanding the fundamental mechanisms for the progression of atherosclerosis-the underlying cause for the vast majority of all cardiovascular (CVD)-related complications. Aging is the dominant risk factor for clinically significant atherosclerotic lesion formation, yet the heightened impact of aging on the disease is not accounted for by changes in traditional risk factors, such as lack of physical activity, smoking, hypertension, hyperlipidemia, or diabetes mellitus. This review will examine the pathological and biochemical processes of atherosclerotic plaque formation and growth, with particular focus on the aging risk vis-a-vis arterial homeostasis. Particular focus will be placed on the impact of a number of important contributors to arterial homeostasis including bone marrow (BM)-derived vascular progenitor cells, differential monocyte subpopulations, and the role of cellular senescence. Finally, this review will explore many critical observations in the way the disease process has been reassessed both by clinicians and researchers, and will highlight recent advances in this field that have provided a greater understanding of this aging-driven disease.
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