Mutations in smooth muscle contractile proteins, including actin, myosin, and tropomyosin, disrupt the contractile cytoskeleton and are strongly linked to diseases such as thoracic aortic aneurysms.
This review provides a comprehensive overview of the smooth muscle contractile cytoskeleton, emphasizing its unique regulatory mechanisms and the role of MYH11 mutations in vascular disease.
Abstract Smooth muscle cells are widespread in the human body, found in a range of tissues from the vasculature to the gut, airways, bladder and so on. They can be found as isolated cells or organised into syncytia (groups of cells). The organisation of the contractile cytoskeleton (smooth muscle actin and myosin filaments) is less well understood than that of striated (cardiac and skeletal) muscle. This review aims to explore what is known, the potential effects of mutations in smooth muscle actin, myosin and tropomyosin and how they lead to disease, and to highlight what we have still to learn about the smooth muscle contractile cytoskeleton.
Carrington et al. (Wed,) conducted a review in Smooth muscle diseases. Mutations in smooth muscle contractile proteins, including actin, myosin, and tropomyosin, disrupt the contractile cytoskeleton and are strongly linked to diseases such as thoracic aortic aneurysms.