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Smooth muscle cell apoptosis in arteriosclerosis
1Institute for Biomedical Aging Research, Austrian Academy of Sciences, Rennweg 10, 6020 Innsbruck, Austria.
Insights
Vascular smooth muscle cell (SMC) apoptosis plays a crucial role in arteriosclerosis development. Understanding the balance between SMC proliferation and apoptosis is key to managing this age-related vascular disease.
Area of Science:
- Cardiovascular Biology
- Pathology
- Biomedical Engineering
Background:
- Arteriosclerosis is an age-related vascular disease involving vascular smooth muscle cell (SMC) accumulation.
- SMC apoptosis is increasingly recognized as a critical factor in arteriosclerosis development and lesion instability.
Purpose of the Study:
- To review the mechanisms and impact of SMC apoptosis in arteriosclerosis pathogenesis.
- To highlight the role of biomechanical stress in SMC apoptosis.
Main Methods:
- Literature review focusing on SMC apoptosis in various forms of arteriosclerosis.
- Analysis of in vitro and in vivo studies on stimuli inducing SMC apoptosis.
- Examination of the interplay between SMC proliferation and apoptosis.
Main Results:
- SMC accumulation and apoptosis are key events in arteriosclerosis.
- Stimuli like oxidized lipoproteins and hemodynamic stress induce SMC apoptosis.
- The balance between SMC proliferation and apoptosis influences vascular remodeling.
Conclusions:
- SMC apoptosis is a significant contributor to arteriosclerosis and lesion instability.
- Biomechanical stress is an important factor in inducing SMC apoptosis.
- Further research into the SMC apoptosis balance may offer clinical implications for atherogenesis.
Abstract:
Arteriosclerosis, a paradigmatic age-related disease, encompasses (spontaneous) atherosclerosis, restenosis after percutaneous transluminal coronary angioplasty, autologous arterial or vein graft arteriosclerosis and transplant arteriosclerosis. In all types of arteriosclerosis, vascular smooth muscle cell (SMC) accumulation in the intima is a key event, but abundant evidence also indicates the importance of SMC apoptosis in the development of arteriosclerosis. Because SMC proliferation and apoptosis coincide in arteriosclerotic lesions, the balance between these two processes could be a determinant during vessel remodeling and disease development. Various stimuli, including oxidized lipoproteins, altered hemodynamic stress and free radicals, can induce SMC apoptosis in vitro. As risk factors for arteriosclerosis, these stimuli may also lead to vascular cell apoptosis in vivo. The presence of apoptotic cells in atherosclerotic and restenotic lesions could have potential clinical implications for atherogenesis and contributes to the instability of the lesion. Based on the progress in this field, this review focuses on the mechanism and impact of SMC apoptosis in the pathogenesis of arteriosclerosis and highlights the role of biomechanical stress in SMC apoptosis.