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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
Loss of bone marrow-derived vascular progenitor cells leads to inflammation and atherosclerosis
Pascal J Goldschmidt-Clermont1
1Department of Medicine, Duke University Medical Center, Duke University Hospital, Durham, NC, USA.
Insights
Aging impairs bone marrow progenitor cells, hindering arterial repair and driving atherosclerosis. This age-related decline in vascular repair contributes to cardiovascular disease and thromboembolic complications.
Area of Science:
- Cardiovascular Science
- Aging Research
- Regenerative Medicine
Background:
- Aging is a primary risk factor for atherosclerosis and related thromboembolic complications.
- The mechanisms underlying age-related arterial wall deterioration are not fully understood.
- Arterial homeostasis is maintained by a repair system involving local and bone marrow-derived cells.
Purpose of the Study:
- To elucidate the role of aging in the failure of bone marrow-derived vascular progenitor cells.
- To explain how this failure contributes to atherosclerosis and its complications.
- To highlight the implications for preventing and treating age-related cardiovascular diseases.
Main Methods:
- Review of existing literature on aging, atherosclerosis, and bone marrow stem cell function.
- Analysis of the interplay between chronic arterial injury, repair mechanisms, and age-dependent changes.
- Integration of data on risk factors like hyperlipidemia and their impact on progenitor cell production.
Main Results:
- Aging leads to a failure in the bone marrow's ability to produce sufficient vascular progenitor cells.
- This age-dependent deficit impairs arterial wall repair and rejuvenation processes.
- The resulting imbalance between arterial injury and repair drives atherosclerotic inflammation and thromboembolic events.
Conclusions:
- Bone marrow and its progenitor cells are critical regulators in the pathogenesis of atherosclerosis.
- Targeting bone marrow function and progenitor cell therapies offers a new dimension for preventing and treating atherosclerosis.
- Understanding this age-related mechanism is crucial for future therapeutic strategies against cardiovascular disease.
Background:
Aging represents the most powerful risk for the development of atherosclerosis and atherosclerotic thromboembolic complications. Yet, the mechanism by which aging affects the arterial wall and its deterioration has remained essentially uncharacterized.
Findings:
Chronic injuries to the arterial wall contribute to the development of atherosclerosis. However, it is important to note that a complex repair system that involves both local and bone marrow-derived cells maintains arterial homeostasis and integrity. With this review, we explain how the age-dependent failure of the bone marrow to produce vascular progenitor cells responsible for such arterial repair--an inability that results from the impact of a lifetime of risk factors such as hyperlipidemia--drives atherosclerosis and its thromboembolic complications. As a consequence of such failure, the normal processes of arterial wall repair and rejuvenation are impaired. The disequilibrium that ensues between injury of the arterial wall and repair leads to atherosclerotic inflammation and consequent thromboembolic complications.
Conclusion:
The bone marrow and derived progenitor cells represent key regulators of atherosclerosis, and progress in the prevention and treatment of atherosclerosis and its thromboembolic complications will need to take into account this new dimension for the disease process.
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