Four and a half Lin11, Isl-1, Mec-3(LIM) domain protein 1 (FHL1) regulates vascular remodeling in low-flow vein grafts

Background: Neointimal hyperplasia (NIH) is a critical determinant of long-term patency of vein grafts following coronary artery bypass grafting (CABG). The development of neointima is influenced by hemodynamic conditions. Our previous studies have demonstrated that four and a half LIM domain protein 1 (FHL1) effectively attenuates neointimal formation in vein grafts under normal flow conditions. However, the role of FHL1 in low-flow hemodynamic environments remains unclear. Elucidating the mechanisms underlying NIH in low-flow settings is essential for improving low-flow vein graft outcomes. Methods: immunofluorescence analysis. FHL1-knockout SD rats and SD rats with adenovirus-mediated FHL1 overexpression were used to evaluate the progression of NIH under low-flow conditions. Results: < 0.01). Conclusion: In low-flow vein grafts, FHL1 may promote favorable vascular remodeling by inhibiting the MAPK signaling pathway, thereby attenuating neointimal cell phenotype switching and mitigating vascular inflammation.