Human Internal Thoracic Artery Smooth Muscle Cells: HITASMC

In vivo, these vascular smooth muscle cells are located within the internal thoracic artery (ITA). The internal thoracic artery arises from the subclavian artery and descends along the inner anterior thoracic wall, deep to the costal cartilages and internal intercostal muscles. It gives rise to pericardiacophrenic artery, anterior intercostal, and perforating branches, and typically ends as the musculophrenic artery (musculophrenic atery) and superior epigastric artery. The internal thoracic artery resides within a vascular bed that is relatively resistant to atherosclerosis. It is well suited to arterial flow and is lined by a highly functional endothelial cell layer that works in tandem with the underlying vascular smc population to maintain structural integrity. This protective vascular microenvironment makes the ITA more resistant to atherosclerosis than many other arterial beds, such as the coronary artery or branches of a posterior intercostal artery, which are far more prone to chronic plaque development. The primary function of HITASMC is to regulate vascular tone and maintain arterial wall elasticity. However, their clinical fame stems from their performance in surgical conduits. The internal thoracic artery is relatively resistant to atherosclerosis and is the preferred arterial conduit for CABG. When utilized as ITA grafts, these vessels display superior long-term patency rates. Unlike other conduits, they exhibit a striking resistance to intimal thickening and downstream vascular occlusion after implantation. In vitro, HITASMC often show lower proliferative and migratory responses to mitogens such as PDGF-BB than smooth muscle cells from more disease-prone vessels, making them useful for studying mechanisms of vascular resilience. Researchers use this passage of cells to study how they regulate intracellular networks—such as the localized coordination of store-operated calcium entry (SOCE) and phosphodiesterases (like PDE1C) at the cell’s leading edge—to prevent the uncontrolled migration that typically drives restenosis in other vessels.