Vascular calcification (VC) is a complex pathological process, which is closely related to chronic kidney disease, atherosclerosis, diabetes and aging. This phenomenon is mainly driven by the convergence of cellular and molecular molecular mechanisms, including osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs), persistent oxidative stress, extracellular vesicle-mediated calcification, and activation of multiple cross-signaling signaling pathways. The multifaceted evidence emphasizes the key role of VSMCs cytoskeleton remodeling in the progression of VC, and establishes a significant link between cytoskeleton dynamics and calcification initiation, which has potential predictive value under specific conditions. This article reviews the factors affecting the remodeling and stability of VSMCs cytoskeleton, focusing on their effects on VSMCs transdifferentiation and calcification. Finally, we highlighted the role of cytoskeleton in the process of cardiovascular calcification, explored strategies for mediating calcification, and proposed potential directions for future research.
Yang et al. (Sun,) studied this question.