Arterial Remodeling: The Role of Mitochondrial Metabolism in Vascular Smooth Muscle Cells.

Arterial remodeling is a common pathological foundation of cardiovascular diseases such as atherosclerosis, vascular restenosis, hypertension, pulmonary hypertension, aortic dissection and aneurysm. Vascular smooth muscle cells (VSMCs) are not only the main cellular components in the middle layer of the arterial wall but also the main cells involved in arterial remodeling. Dedifferentiated VSMCs lose their contractile properties and convert to synthetic, secretory, proliferative, and migratory phenotypes, which play key roles in the pathogenesis of arterial remodeling. As the main site of biological oxidation and energy transformation in eukaryotic cells, mitochondrial numbers and function are very important in maintaining the metabolic processes in VSMCs. Mitochondrial dysfunction and oxidative stress are novel triggers of the phenotypic transformation of VSMCs, leading to the onset and development of arterial remodeling. Therefore, pharmacological measures to improve mitochondrial dysfunction reverse arterial remodeling by improving VSMC metabolic disorders and phenotypic transformation, which brings new options for the treatment of cardiovascular diseases related to arterial remodeling. This review summarizes the relationship between mitochondrial dysfunction and cardiovascular diseases associated with arterial remodeling and then discusses the potential mechanism by which mitochondrial dysfunction participates in pathological arterial remodeling. Furthermore, maintaining or improving mitochondrial function can be a new intervention strategy to prevent the progression of arterial remodeling.