Sulodexide counteracts endothelial dysfunction induced by metabolic or non-metabolic stresses through activation of the autophagic program.
作者: De Felice FMegiorni FPietrantonio ITini PLessiani GMastroiacovo DMattana PAntinozzi CDi Luigi LDelle Monache SAngelucci AFestuccia CFanzani AMaggio RTombolini VGravina G LMarampon F
作者单位: 1Department of Radiotherapy, "Sapienza" University of Rome, Rome, Italy.
刊名: European review for medical and pharmacological sciences, 2019, Vol.23 (6), pp.2669-2680
来源数据库: PubMed Journal
DOI: 10.26355/eurrev_201903_17415
原始语种摘要: OBJECTIVE(#br)Endothelial dysfunction (ED) predisposes to venous thrombosis (VT) and post-thrombotic syndrome (PTS), a long-term VT-related complication. Sulodexide (SDX) is a highly purified glycosaminoglycan with antithrombotic, pro-fibrinolytic and anti-inflammatory activity used in the treatment of chronic venous disease (CVD), including patients with PTS. SDX has recently obtained clinical evidence in the "extension therapy" after initial-standard anticoagulant treatment for the secondary prevention of recurrent deep vein thrombosis (DVT). Herein, we investigated how SDX counteracts ED.(#br)MATERIALS AND METHODS(#br)Human umbilical vein endothelial cells (HUVEC) were used. Metabolic and non metabolic-induced ED was induced by treating with methylglyoxal (MGO) or irradiation (IR),...
全文获取路径: PubMed  (合作)

  • induced 感应的
  • metabolic 新陈代谢的
  • activation 活化
  • dysfunction 功能障碍
  • secondary 二次的
  • endothelial 内皮的
  • prevention 妨碍
  • methylglyoxal 丙酮醛
  • autophagy 自体消瘦
  • inflammatory 激怒的