Molecular Mechanisms of Vascular Conduit Remodeling in Coronary Artery Bypass Grafting: Implications for Long-Term Graft Patency

Coronary artery bypass grafting (CABG) remains an important surgical treatment for patients with complex coronary artery disease; however, its long-term success depends substantially on graft patency. This narrative review examines the structural, cellular, and molecular mechanisms potentially contributing to vascular conduit adaptation, remodeling, and graft durability following CABG, with particular emphasis on the internal thoracic artery and saphenous vein. The review discusses endothelial homeostasis, KLF2/KLF4–eNOS–NO signaling, oxidative stress, inflammatory activation, vascular smooth muscle cell phenotypic switching, and extracellular matrix remodeling. Particular attention is given to signaling pathways involving NF-κB, PDGF-BB, TGF-β, Akt, RhoA/ROCK, MAPK, and JAK2/STAT3, as well as matrix metalloproteinases and regulatory non-coding RNAs. Comparative analyses of human vascular tissues and isolated cells have identified molecular and cellular differences that may contribute to the distinct responses of vascular conduits to arterial hemodynamic conditions. However, direct molecular evidence from human CABG grafts remains limited, and much of the available mechanistic knowledge is derived from analyses of harvested human vascular tissues, isolated cell models, ex vivo arterialization experiments, and animal studies. Consequently, these findings should not be interpreted as direct evidence that specific molecular pathways determine long-term graft patency in patients undergoing CABG. Moreover, conduit-specific molecular evidence remains substantially more extensive for the internal thoracic artery and saphenous vein than for other arterial conduits. A better understanding of these mechanisms, supported by prospective studies integrating molecular findings with clinical and imaging outcomes, may facilitate the identification of clinically relevant biomarkers and potential therapeutic targets to improve graft patency.