ArticlePeerJ2026
Four and a half Lin11, Isl-1, Mec-3(LIM) domain protein 1 (FHL1) regulates vascular remodeling in low-flow vein grafts.
Article in PeerJ, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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: The vein graft model was established in Sprague-Dawley (SD) rats, with low blood flow induced by ligation of the internal carotid artery. Then eointimal area was quantified using histological staining, while the expression of neointimal markers was assessed Results: Following internal carotid artery ligation, the mean blood flow velocity in the vein grafts decreased immediately ( 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.
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