Low molecular weight (LMW) heparin inhibits injury-induced femoral artery remodeling in mouse via upregulating CD44 expression

Angioplasty is widely used in clinical practice to treat various stenostic vascular disorders, but the postangioplasty reocclusion has been a big limit and the mechanism underlying the vascular remodeling remains poorly understood. LMW heparin has been a promising medicine to inhibit VSMC proliferation. However, the mechanism of LMW heparin inhibition against smooth muscle cell (SMC) proliferation and its clinical usefulness is still not clear. Our present data, which were based on in vivo and in vitro studies, suggested that LMW heparin induced higher CD44 expression in VSMCs, and through the CD44 pathway, LMW heparin significantly reduced SMC proliferation and injury-induced femoral artery remodeling. Our study clarified the roles of LMW heparin in vascular occlusive diseases. This study helps to elucidate the underlying cellular and molecular mechanism by which LMW heparin inhibits injury-induced remodeling and could promote creating new therapeutics to control the exaggerated neointimal hyperplasia.