C3 or not C3: that is the question.

Numerous investigators have studied the potential genetic causes of essential hypertension, and several genes have been described as candidates.1,2 These genes may contribute to the inappropriate and exaggerated growth of arterial smooth muscle cells in genetically hypertensive individuals and thus ultimately contribute to the disease by supporting creation of stronger, more muscular, and sometimes narrowed arteries. The article by Lin et al in this issue of Hypertension3 describes selective expression of the complement protein complement 3 (C3) in arterial cells from the spontaneously hypertensive rat (SHR) and clear involvement of this protein in mediating enhanced arterial smooth muscle growth in the SHR.