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Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
Aging, smooth muscle cells and vascular pathobiology: implications for atherosclerosis
Augusto Orlandi1, Marie-Luce Bochaton-Piallat, Giulio Gabbiani
1Anatomic Pathology Institute, Department of Biopathology, Tor Vergata University of Rome, Via Montpellier 1, Rome, Italy. orlandi@uniroma2.it
Aging is an independent risk factor for atherosclerosis, promoting arterial wall changes. Smooth muscle cell (SMC) migration and altered behavior in aged arteries contribute to vascular remodeling and disease progression.
Area of Science:
- Vascular Biology
- Gerontology
- Cardiovascular Disease
Background:
- Epidemiological and autopsy studies link aging to atherosclerosis.
- Aged arteries show increased susceptibility to atherogenetic stimuli.
- Aging is considered an independent atherogenetic risk factor.
Purpose of the Study:
- Investigate the role of aging in atherosclerosis.
- Examine changes in arterial smooth muscle cells (SMCs) with aging.
- Understand biomolecular mechanisms of vascular aging.
Main Methods:
- Review of epidemiological and autopsy studies.
- Analysis of experimental data on aged subjects.
- Focus on smooth muscle cell (SMC) behavior and phenotype changes.
Main Results:
- Aging promotes SMC migration from tunica media to tunica intima.
- Intimal SMC accumulation leads to myointimal thickening and lesion progression.
- SMC phenotype shifts to synthetic, with altered proliferation, apoptosis, and growth factor response.
Conclusions:
- Altered SMC properties are crucial in vascular aging and atherosclerosis.
- Understanding these mechanisms can inform strategies against vascular aging.
- Targeting SMC pathobiology may mitigate atherosclerosis progression.
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