期刊文献+

激活素A与心脏疾病关系的研究进展 被引量:1

Research Progress of Activin A and Heart Diseases
下载PDF
导出
摘要 激活素A与急性及慢性炎症有关并可用于预测疾病的严重性,激活素A也参与纤维化和凋亡等疾病的病理过程。在不同的疾病模型中,抑制激活素A能够减弱机体的炎症反应、逆转纤维化及降低病死率。心脏疾病的发生、发展及预后与炎症、纤维化和凋亡有密切关系,同时激活素A在很多心脏疾病中发挥重要作用。因此,激活素A已经成为诊断和治疗心脏疾病的一种工具。 Activin A is related to acute and chronic inflammation and can be used to predict the severity of the diseases. Activin A is also involved in the pathological process of fibrosis and apoptosis. In various dis- eases models,inhibition of activin A can attenuate inflammation, fibrosis, apoptosis and mortality. The devel- opment and prognosis of heart diseases are tightly associated with inflammation, fibrosis and apoptosis, and activin A plays an important role in many heart diseases. Therefore activin A is regarded as a diagnostic and therapeutic tools in various heart diseases.
出处 《医学综述》 2016年第17期3340-3343,共4页 Medical Recapitulate
基金 湖北省自然科学基金(2013CFA117)
关键词 心脏疾病 激活素A 炎症 纤维化 凋亡 Heart disease Activin A Inflammation Fibrosis Apoptosis
  • 相关文献

参考文献2

二级参考文献17

  • 1Zhao ZQ, Corvera JS, Halkos ME, et al. Inhibition of myocardial injury by ischemie posteonditioning during reperfusion: comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol,2003;285(2): H579-588.
  • 2Sun HY, Wang NP, Halkos M, et al. Posteonditioning attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen-actlvated protein kinase signaling pathways. Apoptosis,2006,11(9):1583-1593.
  • 3Kloner RA, Dow J, Bhandari A. Postconditioning markedly attenuates ventricular arrhythmias after ischemia-reperfusion. J Cardiovasc Pharmacol Ther, 2006 , 11 (1):55-63.
  • 4Zhu M, Feng J, Lucchinetti E, et al. Isehemie posteonditioning protects remodeled myocardium via the PI3K-PKB/Akt reperfusion injury salvage kinase pathway. Cardiovasc Res, 2006, 72(1):152-162.
  • 5Maeshima A, Nojima Y, Kojima I. Aetivin A; an autoerine regulator of cell growth and differentiation in renal proximal tubular cells. Kidney Int,2002,62(2) :446-454.
  • 6Bagdatoglu OT, Polat G, Bagdatoglu C, et al. Effects of Peripheral Nerve Ischemia-Reperfusion Model on Serum Cytokine Levels. Turk Neurosurg,2008 ; 18(2):149-156.
  • 7Argaud L, Gateau-Roesch O, Augeul L, et al. Increased mitochondrial calcium coexists with decreased reperfusion injury in postcondltioned (but not preconditioned) hearts. Am J Physiol Heart Circ Physiol,2008,294(1):H386-391.
  • 8Goodman MD, Koch SE, Fuller-Biter GA, et al. Regulating RISK : a role for JAK-STAT signaling in postconditionlng? Am J PhysioI Heart Cite Physlol, 2008 ,295(4) : H1649-1656.
  • 9Cohen MV, Yang XM, Downey JM. Acidosis, oxygen, and interference with mitochondrial permeability transition pore formation in the early minutes of reperfusion are critical to postconditionings success. Basic Res Cardiol, 2008; 103 (5) : 464-471.
  • 10FlorholmenG, Halvorsen B, BerakiK, etal. ActivinAinhibits organization of sarcomeric proteins in cardlomyocytes induced by leukemia inhibitory factor. J Mol Cell Cardiol,2006 41(4):689-697.

共引文献6

同被引文献2

引证文献1

二级引证文献2

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