[HTML][HTML] Control of phenotypic plasticity of smooth muscle cells by bone morphogenetic protein signaling through the myocardin-related transcription factors
Vascular smooth muscle cells (VSMCs), unlike other muscle cells, do not terminally
differentiate. In response to injury, VSMCs change phenotype, proliferate, and migrate as
part of the repair process. Dysregulation of this plasticity program contributes to the
pathogenesis of several vascular disorders, such as atherosclerosis, restenosis, and
hypertension. The discovery of mutations in the gene encoding BMPRII, the type II subunit of
the receptor for bone morphogenetic proteins (BMPs), in patients with pulmonary arterial …
differentiate. In response to injury, VSMCs change phenotype, proliferate, and migrate as
part of the repair process. Dysregulation of this plasticity program contributes to the
pathogenesis of several vascular disorders, such as atherosclerosis, restenosis, and
hypertension. The discovery of mutations in the gene encoding BMPRII, the type II subunit of
the receptor for bone morphogenetic proteins (BMPs), in patients with pulmonary arterial …