期刊文献+

Forkhead box M1 transcription factor:a novel target for pulmonary arterial hypertension therapy 被引量:2

原文传递
导出
摘要 Background Forkhead box M1(FoxM1),a member of forkhead family,plays a key role in carcinogenesis,progression,invasion,metastasis and drug resistance.Based on the similarities between cancer and pulmonary arterial hypertension,studies on the roles and mechanisms of FoxM1 in pulmonary arterial hypertension have been increasing.This article aims to review recent advances in the mechanisms of signal transduction associated with FoxM1 in pulmonary arterial hypertension.Data sources Articles were retrieved from PubMed and MEDLINE published after 1990,including-but not limited to FoxM1 and pulmonary arterial hypertension.Results FoxM 1 is overexpressed in pulmonary artery smooth muscle cells in both pulmonary arterial hypertension patients and animal models,and promotes pulmonary artery smooth muscle cell proliferation and inhibits cell apoptosis via regulating cell cycle progression.Multiple signaling molecules and pathways,including hypoxia-inducible factors,transforming growth factor-β/Smad,SET domain-containing 3/vascular endothelial growth factor,survivin,cell cycle regulatory genes and DNA damage response network,are reported to cross talk with FoxM1 in pulmonary arterial hypertension.Proteasome inhibitors are effective in the prevention and treatment of pulmonary arterial hypertension by inhibiting the expression and transcriptional activity of FoxM1.Conclusions FoxM1 has a crucial role in the pathogenesis of pulmonary arterial hypertension and may represent a novel therapeutic target.But more details of interaction between FoxM1 and other signaling pathways need to be clarified in the future.
出处 《World Journal of Pediatrics》 SCIE CAS CSCD 2020年第2期113-119,共7页 世界儿科杂志(英文版)
  • 相关文献

参考文献1

二级参考文献117

  • 1Devereux RB, Lyle PA. Losartan for the treatment of hypertension and left ventricular hypertrophy: the Losartan intervention for endpoint reduction in hypertension (LIFE) study. Expert Opin Pharmacother 2004; 5:2311-2320.
  • 2Parker TG, Packer SE, Schneider MD. Peptide growth factors can provoke "fetal" contractile protein gene expression in rat cardiac myocytes. J Clin Invest 1990; 85:507-514.
  • 3Rosenkranz S, Flesch M, Amann K, et al. Alterations of β- adrenergic signaling and cardiac hypertrophy in transgenic mice overexpressing TGF-β1. Am J Physiol Heart Circ Physiol2002; 283:H1253-1262.
  • 4Goumans M J, Zonneveld A J, ten Dijke E TGFβ-induced endothelial to mesenchymal transition; a switch to cardiac fibrosis? Trends Cardiovase Med, in press.
  • 5Larsson J, Goumans M J, Sjostrand L J, et al. Abnormal angiogenesis but intact hematopoietic potential in TGF-β type Ⅰ receptor-deficient mice. EMBO J 2001; 20:1663-1673.
  • 6Guttmacher AE, Marchuk DA, White RI Jr. Hereditary hemorrhagic telangiectasia. N Engl J Med 1995; 333:918-924.
  • 7Heldin C-H, Miyazono K, ten Dijke P. TGF-β signalling from cell membrane to nucleus through SMAD proteins. Nature 1997; 390:465-471.
  • 8Shi Y, Massague J. Mechanisms of TGF-β signaling from cell membrane to the nucleus. Cell 2003; 113:685-700.
  • 9Schmierer B, Hill CS. TGFβ-SMAD signal transduction: molecular specificity and functional flexibility. Nat Rev Mol Cell Biol2007; 8:970-982.
  • 10ten Dijke P, Arthur HM. Extracellular control of TGFβ signalling in vascular development and disease. Nat Rev Mol Cell Biol2007; 8:857-869.

共引文献30

同被引文献12

引证文献2

二级引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部