A role for an alternatively spliced Id3 isoform in vascular lesions?

Alterations in proliferation, migration, and function of vascular smooth muscle cells (SMCs) are important in the formation of atherosclerotic and restenotic lesions.1 Although of tremendous clinical importance, the precise molecular mechanisms controlling the proliferation and differentiation of SMCs are not completely understood. Regulation of growth and differentiation in skeletal and cardiac muscle involves a class of transcription factors called helix-loop-helix (HLH) proteins, but the situation in smooth muscle is less clear. The study by Matsumura et al2 in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology investigates a particular HLH protein in vascular SMCs in culture and in vivo after vascular injury.