期刊文献+

TXNIP介导的氧化应激在疾病中的作用机制 被引量:25

Action and mechanism of oxidative stress mediated by TXNIP in diseases
下载PDF
导出
摘要 硫氧还蛋白相互作用蛋白(TXNIP)通过与硫氧还蛋白(Trx)的结合而抑制Trx的抗氧化作用,促进了活性氧簇(ROS)的产生与积聚,诱发内质网应激与线粒体应激,最终可诱导炎症或细胞凋亡。TXNIP所介导的氧化应激在糖尿病及其并发症(糖尿病肾病、糖尿病视网膜病变等)、动脉粥样硬化、缺血/再灌注损伤、癌症(肝细胞癌、膀胱癌、乳腺癌、白血病)等疾病的发生、发展过程中起着重要的调控作用。该文就TXNIP介导的氧化应激在相关疾病中的作用机制及研究进展进行综述。 Thioredoxin-interacting protein( TXNIP) suppresses the antioxidative function of thioredoxin( Trx) by combining with thioredoxin( Trx). Therefore,it promotes the generation and accumulation of reactive oxygen species( ROS),inducing endoplasmic reticulum stress and mitochondrial stress,which leads to cellular inflammation or cellular apoptosis ultimately.TXNIP-mediated oxidative stress plays a crucial role in controlling the generation and development of some diseases,such as diabetes and its complications( diabetic nephropathy diabetic retinopathy etc.),atherosclerosis ischemia/reperfusion injury,cancers( hepatocellular carcinoma,carcinoma of urinary bladder,mammary cancer,leukemia) etc. Here,we try to review the action and mechanism of oxidative stress mediated by TXNIP in the diseases and the progress in research.
出处 《中国药理学通报》 CAS CSCD 北大核心 2018年第1期16-19,共4页 Chinese Pharmacological Bulletin
基金 国家自然科学基金资助项目(No 81673814) 广东省科技计划项目(No 2016A020215148) 广东省医学科研基金(No A2016293)
关键词 硫氧还蛋白相互作用蛋白(TXNIP) 氧化应激 线粒体应激 内质网应激 细胞炎症 细胞凋亡 thioredoxin-interacting protein(TXNIP) oxidative stress mitochondrial stress endoplasmic reticulum stress cellular inflammation cellular apoptosis
  • 相关文献

参考文献4

二级参考文献55

  • 1Twig G, Elorza A, Molina A J, Mohamed H, Wikstrom JD, Walzer G, et al. Fission and selective fusion govern mitochondrial segrega- tion and elimination by autophagy. EMBO J 2008; 27(2): 433-46.
  • 2Yoon Y, Galloway CA, Jhun BS, Yu T. Mitochondrial dynamics in diabetes. Antioxid Redox Signal 2011; 14(3): 439-57.
  • 3Pletjushkina OY, Lyamzaev KG, Popova EN, Nepryakhina OK, Ivanova OY, Domnina LV, et al. Effect of oxidative stress on dy- namics of mitochondrial reticulum. Biochim Biophys Acta 2006; 1757(5-6): 518-24.
  • 4Jahani-Asl A, Pilon-Larose K, Xu W, MacLaurin JG, Park DS, McBride HM, et al. The mitoehondrial inner membrane GTPase, optic atrophy 1 (Opal), restores mitochondrial morphology and promotes neuronal survival following excitotoxicity. J Biol Chem 2011; 286(6): 4772-82.
  • 5Wasiak S, Zunino R, McBride HM. Bax/Bak promote sumoyla- tion of DRPI and its stable association with mitochondria during apoptotic cell death. J Cell Biol 2007; 177(3): 439-50.
  • 6Brooks C, Wei Q, Feng L, Dong G, Tao Y, Mei L, et al. Bak reg- ulates mitochondrial morphology and pathology during apoptosis by interacting with mitofusins. Proc Natl Acad Sci USA 2007; 104(28): 11649-54.
  • 7Lacza Z, Puskar M, Figueroa JP, Zhang J, Rajapakse N, Busija DW. Mitochondrial nitric oxide synthase is constitutively active and is functionally upregulated in hypoxia. Free Radio Biol Med 2001; 31(12): 1609-15.
  • 8Taha R, Seidman E, Mailhot G, Boudreau F, Gendron FP, Beau- lieu JF, et al. Oxidative stress and mitochondrial functions in the intestinal Caco-2/15 cell line. PLoS One 20 l 0; 5(7): e 11817.
  • 9Paradies G, Petrosillo G, Paradies V, Ruggiero FM. Role of car- diolipin peroxidation and Ca2+ in mitochondrial dysfunction and disease. Cell Calcium 2009; 45(6): 643-50.
  • 10Sect RC, Lee CY, Lira EC, Tan J J, Quek AM, Chong WL, et al. Oxidative damage in Parkinson disease: Measurement using ac- curate biomarkers. Free Radie Biol Med 2010; 48(4): 560-6.

共引文献58

同被引文献211

引证文献25

二级引证文献113

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