Brian R. Wamhoff

TL;DR: The focus of this review is to provide an overview of the current state of knowledge of molecular mechanisms/processes that control differentiation of vascular smooth muscle cells (SMC) during normal development and maturation of the vasculature, as well as how these mechanisms/ processeses are altered in vascular injury or disease.

TL;DR: The unique biological properties of Mox macrophages suggest this phenotype may play an important role in atherosclerotic lesion development as well as in other settings of chronic inflammation.

TL;DR: Results provide compelling evidence that myocardin plays a key role as a transcriptional coactivator of SMC marker genes through CArG-dependent mechanisms.

TL;DR: It is reported that SMC-restricted binding of SRF to murine SMC gene CArG box chromatin is associated with patterns of posttranslational histone modifications within this chromatin that are specific to the SMC lineage in culture and in vivo, including methylation and acetylation to histone H4 residues.

TL;DR: Current knowledge in vascular smooth muscle cell phenotypic modulation is summarized and some of the key unresolved challenges and questions requiring further study are identified.