Myocardin--not quite MyoD.

Smooth muscle cells (SMCs) have evolved to subserve a variety of diverse functions in higher vertebrates, including modulation of arterial tone, regulation of airway resistance, and control of gastrointestinal motility. The diverse functional capacities of SMCs are ultimately determined by the expression of genes encoding SMC-restricted contractile and cytoskeletal proteins, intracellular enzymes, cell surface ligands, and receptors. Several features distinguish the SMC lineage from the skeletal (fast and slow) and cardiac muscle cell lineages. In contrast to skeletal and cardiac muscle cells, SMCs fail to undergo terminal differentiation and permanently exit the cell cycle. In addition, SMCs retain the capacity to reversibly modulate their phenotype during postnatal development in response to a variety of extracellular stimuli including vessel wall injury. As such, the molecular programs underlying SMC differentiation must differ fundamentally from those programs governing skeletal and cardiac myocyte differentiation.