期刊文献+
任意字段
题名或关键词
题名
关键词
文摘
作者
第一作者
机构
刊名
分类号
参考文献
作者简介
基金资助
栏目信息

瞬时受体电位阳离子通道蛋白6在肾小球足细胞损伤中的作用 被引量：1

Role of Transient Receptor Potential Cation Channel 6 in Podocyte Injury
原文传递
导出
摘要 瞬时受体电位阳离子通道蛋白6(TRPC6)是新近发现的肾小球足细胞分子,定位于足细胞裂孔隔膜,与nephrin、podocin和CD2AP存在共定位分布,共同参与信号转导,并维持足细胞正常的结构和功能。TRPC6基因突变可以导致常染色体显性家族性局灶节段性肾小球硬化,患者表现为大量蛋白尿和足细胞损伤,体外试验也表明其高表达可通过增加钙离子内流损伤足细胞,说明TRPC6与蛋白尿的发生、发展密切相关。现将阐明TRPC6在足细胞损伤中的作用,有望为肾脏病的诊断和治疗提供新的靶点。 Recent studies have shown that transient receptor potential cation channel 6（TRPC6） expressed in podocytes,and located in slit diaphragm,it colocalized with nephrin,podocin and CD2AP,participating in signal transduction and maintaining podocytes normal construction and function.Mutations in TRPC6 cause autosomal dominant familial focal segmental glomerulosclerosis which is characterized by grade proteinuria and podocyte injury.In vitro studies,it also indicates that overexpression of TRPC6 leads to podocyte dysfunction,maybe through elevating calcium influx,suggesting that TRPC6 associates with the onset and development of proteinuria.This article will describe the role of TRPC6 in podocyte injury,maybe provide us the new targets for diagnosing and theraping renal disorders in the future.
作者 马媛媛 于力
机构地区 广州医学院附属广州市第一人民医院儿科
出处 《实用儿科临床杂志》 CAS CSCD 北大核心 2012年第5期369-371,共3页 Journal of Applied Clinical Pediatrics
基金 广州市科技计划项目(2010Y1-C521)
关键词 瞬时受体电位阳离子通道蛋白6 足细胞 蛋白尿 transient receptor potential cation channel 6 podocyte proteinuria
分类号 R692 [医药卫生—泌尿科学]
  • 相关文献

参考文献23

  • 1Schlndorff J,Del Camino D,Carrasquillo R,et al.TRPC6 mutations as-sociated with focal segmental glomerulosclerosis cause constitutive acti-vation of NFAT-dependent transcription[J].Am J Physiol Cell Phy-siol,2009,296(3):C558-C569.
  • 2Canaud G,Martinez F,Nol LH,et al.Therapeutic approach to focal andsegmental glomerulosclerosis recurrence in kidney transplant recipients[J].Transplant Rev(Orlando),2010,24(3):121-128.
  • 3Krall P,Canales CP,Kairath P,et al.Podocyte-specific overexpressionof wild type or mutant trpc6 in mice is sufficient to cause glomerular di-sease[J].PLoS One,2010,5(9):e12859.
  • 4Gigante M,Caridi G,Montemurno E,et al.TRPC6 mutations in childrenwith steroid-resistant nephrotic syndrome and atypical phenotype[J].Clin J Am Soc Nephrol,2011,6(7):1626-1634.
  • 5Kanda S,Harita Y,Shibagaki Y,et al.Tyrosine phosphorylation-de-pendent activation of TRPC6 regulated by PLC-γ1 and nephrin:Effectof mutations associated with focal segmental glomerulosclerosis[J].MolBiol Cell,2011,22(11):1824-1835.
  • 6Thilo F,Liu Y,Loddenkemper C,et al.VEGF regulates TRPC6 channelsin podocytes[J].Nephrol Dial Transplant,2011[Epub ahead of print].
  • 7Dionisio N,Albarran L,Berna-Erro A,et al.Functional role of thecalmodulin-and inositol 1,4,5-trisphosphate receptor-binding(CIRB)site of TRPC6 in human platelet activation[J].Cell Signal,2011,23(11):1850-1856.
  • 8Zhu B,Chen N,Wang ZH,et al.Identification and functional analysis ofa novel TRPC6 mutation associated with late onset familial focal segmen-tal glomerulosclerosis in Chinese patients[J].Mutat Res,2009,664(1-2):84-90.
  • 9Reiser J,Polu KR,Mller CC,et al.TRPC6 is a glomerular slit dia-phragm-associated Channel required for normal renal function[J].NatGenet,2005,37(7):739-744.
  • 10Winn MP,Conlon PJ,Lynn KL,et al.A mutation in the TRPC6 cationchannel causes familial focal segmental glomerulosclerosis[J].Scie-nce,2005,308(5729):1801-1804.

同被引文献20

  • 1Reiser J, Polu KR, Moller CC, et al. TRPC6 is a glomerular slit diaphragm- associated channel required for normal renal function[J]. Nat Genet, 2005, 37: 739-744.
  • 2Mukerji N, Damodaran TV, Winn MP. TRPC6 and FSGS: the latest TRP channelopath[J]. Biochim Biophys Acta, 2007, 1772: 859-868.
  • 3Moller CC, Wei C, Altintas MM, et al. Induction of TRPC6 channel in acquired forms of proteinuric kidney disease[J]. J Am Soc Nephrol, 2007, 18 : 29-36.
  • 4Nijenhuis T, Sloan AJ, Hoenderop JG, et al. Angiotensin II contributes to podocyte injury by increasing TRPC6 expression via an NFAT-mediated positive feedback signaling pathway[J]. Am J Pathol, 2011, 179: 1719-1732.
  • 5Jiang L, Ding J, Tsai H, et al. Over- expressing transient receptor potential cation Channel 6 in podocytes induces cytoskeleton rearrangement through increases of intracellular Ca2+ and RhoA activation[J]. Exp Biol Med (Maywood), 2011, 236: 184-193.
  • 6Heeringa SF, Mtiller CC, Du J, et al. A novel TRPC6 mutation that causes childhood FSGS[J]. PLoS One, 2009, 4: e7771.
  • 7Schlsndorff J, De1 Camino D, Carrasquillo R, et al. TRPC6 mutations associated with focal segmental glomerulosclerosis cause constitutive activation of NFAT-dependent transcription [J]. Am J Physiol Cell Physiol, 2009, 296: C558-C569.
  • 8Zhang H, Ding J, Fan Q, et al. TRPC6 up-regulation in Ang II- induced podocyte apoptosis might result from ERK activation and NF-kappaB translocation[J]. Exp Biol Med (Maywood), 2009, 234: 1029-1036.
  • 9Chiluiza D, Krishna S, Schumacher VA, et al. Gain-of-function mutations in transient receptor potential C6 (TRPC6) activate extracellular signal-regulated kinases 1/2 (ERK1/2) [J]. J Biol Chem, 2013, 288: 18407-18420.
  • 10Pippin JW, Brinkkoetter PT, Cormack- Aboud FC, et al. Inducible rodent models of acquired podoeyte diseases[J]. Am J Physiol Renal Physiol, 2009, 296: F213-F229.

引证文献1

二级引证文献3

实用儿科临床杂志
2012年 第5期

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