Implications of autophagy for vascular smooth muscle cell function and plasticity |
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| Affiliation: | 1. Diabetes and Obesity Center, Institute of Molecular Cardiology, University of Louisville School of Medicine, Louisville, KY 40202, USA;2. Department of Biochemistry and Molecular Biology, University of Louisville School of Medicine, Louisville, KY 40202, USA;3. Department of Physiology and Biophysics, University of Louisville School of Medicine, Louisville, KY 40202, USA;1. Institute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, University of South China, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang 421001, Hunan, China;2. Department of Laboratory Animal Science, University of South China, Hengyang 421001, Hunan, China;3. Department of Biochemistry and Molecular Biology, The Libin Cardiovascular Institute of Alberta, Cumming School of Medicine, The University of Calgary, Health Sciences Center, 3330 Hospital Dr NW, Calgary T2N 4N1, Alberta, Canada;1. Laboratory Diagnostics Department, The Haerbin Medical University, 150001, China;2. Laboratory Diagnostics Department, The First Clinic Hospital Affiliated to Haerbin Medical University, 150001, China;1. Department of Biochemistry and Molecular Biology, Hebei Medical University, Zhongshan East Road, Shijiazhuang 050017, China;2. Hebei Center for Disease Control and Prevention, Shijiazhuang 050000, China;3. Department of Urinary Surgery, Second Hospital of Hebei Medical University, Pingan Road, Shijiazhuang 050000, China;4. Third Hospital of Shijiazhuang, Shijiazhuang 050000, China;1. Heart Center, The Third Central Hospital of Tianjin, Tianjin Key Laboratory of Extracorporeal Life Support for Critical Diseases, Artificial Cell Engineering Technology Research Center, Tianjin, 300170, China;1. Robarts Research Institute, London, Ontario, Canada;2. Departments of Medicine (Cardiology), Biochemistry, and Medical Biophysics, University of Western Ontario, London Health Sciences Centre, London, Ontario, Canada |
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| Abstract: | Vascular smooth muscle cells (VSMCs) are fundamental in regulating blood pressure and distributing oxygen and nutrients to peripheral tissues. They also possess remarkable plasticity, with the capacity to switch to synthetic, macrophage-like, or osteochondrogenic phenotypes when cued by external stimuli. In arterial diseases such as atherosclerosis and restenosis, this plasticity seems to be critical and, depending on the disease context, can be deleterious or beneficial. Therefore, understanding the mechanisms regulating VSMC phenotype and survival is essential for developing new therapies for vascular disease as well as understanding how secondary complications due to surgical interventions develop. In this regard, the cellular process of autophagy is increasingly being recognized as a major player in vascular biology and a critical determinant of VSMC phenotype and survival. Although autophagy was identified in lesional VSMCs in the 1960s, our understanding of the implications of autophagy in arterial diseases and the stimuli promoting its activation in VSMCs is only now being elucidated. In this review, we highlight the evidence for autophagy occurring in VSMCs in vivo, elaborate on the stimuli and processes regulating autophagy, and discuss the current understanding of the role of autophagy in vascular disease. |
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| Keywords: | Atherosclerosis Restenosis Hypertension Oxidative stress Cardiovascular Proliferation Free radicals |
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