活性氧在草酸钙肾结石形成中作用机制的研究进展

韩博, 王锐, 安瑞华. 活性氧在草酸钙肾结石形成中作用机制的研究进展[J]. 临床泌尿外科杂志, 2019, 34(4): 319-321,326. doi: 10.13201/j.issn.1001-1420.2019.04.017
引用本文: 韩博, 王锐, 安瑞华. 活性氧在草酸钙肾结石形成中作用机制的研究进展[J]. 临床泌尿外科杂志, 2019, 34(4): 319-321,326. doi: 10.13201/j.issn.1001-1420.2019.04.017
HAN Bo, WANG Rui, AN Ruihua. Advances in research on the mechanism of action of reactive oxygen species in the formation of calcium oxalate kidney stones[J]. J Clin Urol, 2019, 34(4): 319-321,326. doi: 10.13201/j.issn.1001-1420.2019.04.017
Citation: HAN Bo, WANG Rui, AN Ruihua. Advances in research on the mechanism of action of reactive oxygen species in the formation of calcium oxalate kidney stones[J]. J Clin Urol, 2019, 34(4): 319-321,326. doi: 10.13201/j.issn.1001-1420.2019.04.017

活性氧在草酸钙肾结石形成中作用机制的研究进展

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    通讯作者: 安瑞华,E-mail:ruihuaan@126.com
  • 中图分类号: R692.4

Advances in research on the mechanism of action of reactive oxygen species in the formation of calcium oxalate kidney stones

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  • 肾结石的成分繁多、成因复杂,其形成过程一直都是研究者们亟于攻克的领域。随着草酸钙肾结石形成研究的逐步深入,活性氧(ROS)影响草酸钙肾结石形成的部分机制也开始变得明确。本文主要就草酸及草酸钙晶体如何介导形成ROS以及其在草酸钙肾结石形成及防治中相关机制的基础研究作一综述。
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  • [1]

    邓华,杨义,陆丽兰,等.结石类型与年龄、性别的相关性研究[J].临床泌尿外科杂志,2018,33(12):968-971.

    [2]

    吴浩然,胡波,施国伟.草酸钙结晶-肾小管细胞损伤机制研究进展[J].临床泌尿外科杂志,2014,29(4):365-367.

    [3]

    Lu M,Gong X.Upstream reactive oxidative species(ROS)signalsin exogenous oxidative stress-induced mitochondrial dysfunction[J].Cell Biol Int,2009,33(6):658-664.

    [4]

    Sareila O,Kelkka T,Pizzolla A,et al.NOX2 complex-derived ROS as immune regulators[J].Antioxid Redox Signal,2011,15(8):2197-2208.

    [5]

    Joshi S,Peck A B,Khan S R.NADPH Oxidase as a TherapeuticTarget for Oxalate Induced Injury in Kidneys[J].Oxid Med Cell Longev,2013,2013:462361.

    [6]

    Kowluru R A,Kowluru A,Mishra M,et al.Oxidative stress andepigenetic modifications in the pathogenesis of diabetic retinopathy[J].Prog Retin Eye Res,2015,48:40-61.

    [7]

    Perumal Vijayaraman K,Muruganantham S,Subramanian M,et al.Silymarin attenuates benzo(a)pyrene induced toxicity by mitigating ROS production,DNA damage and calcium mediated apoptosis inperipheral blood mononuclear cells(PBMC)[J].Ecotoxicol Environ Saf,2012,86:79-85.

    [8]

    Song C,Mitter S K,Qi X,et al.Oxidative stress-mediated NF-KBphosphorylation upregulates p62/ SQSTM1 and promotes retinal pigmentedepithelial cell survival through increased autophagy[J].PLoS One,2017,12(2):e0171940.

    [9]

    Bodakhe K S,Namdeo K P,Patra K C,et al.A polyherbal formulation attenuates hyperoxaluria-induced oxidative stress and prevents subsequent deposition of calcium oxalate crystals and renal cell injury in rat kidneys[J].Chin J Nat Med,2013,11(5):466-471.

    [10]

    Yu L,Gan X,Liu X,et al.Calcium oxalate crystals induces tight junction disruption in distal renal tubular epithelial cells by activating ROS/Akt/p38 MAPK signaling pathway[J].Ren Fail,2017,39(1):440-451.

    [11]

    Abhishek A,Benita S,Kumari M,et al.Molecular analysis of oxalate-induced endoplasmic reticulum stress mediated apoptosis in the pathogenesis of kidney stone disease[J].J Physiol Biochem,2017,73(4):561-573.

    [12]

    Zuo J,Khan A,Glenton P A,et al.Effect of NADPH oxidase inhibition on theexpression of kidney injury molecule and calcium oxalate crystal deposition inhydroxy-L-proline-induced hyperoxaluria in the male Sprague-Dawley rats[J].Nephrol Dial Transplant,2011,26(6):1785-1796.

    [13]

    Qin B,Wang Q,Lu Y,et al.Losartan Ameliorates Calcium Oxalate-Induced Elevation of Stone-Related Proteins in Renal Tubular Cells by Inhibiting NADPH Oxidase and Oxidative Stress[J].Oxid Med CellLongev,2018,2018:1271864.

    [14]

    Piera-Velazquez S,Makul A,Jiménez SA.Increased expression of NAPDH oxidase 4 in systemic sclerosis dermal fibroblasts:regulation by transforminggrowth factor β[J].Arthritis Rheumatol,2015,67(10):2749-2758.

    [15]

    Li A,Wang J,Zhu D,et al.Arctigenin suppresses transforming growth factor-β1-induced expression of monocyte chemoattractant protein-1 and the subsequent epithelial-mesenchymal transition through reactive oxygen species-dependent ERK/NF-κB signaling pathway in renal tubular epithelial cells[J].Free Radic Res,2015,49(9):1095-1113.

    [16]

    Rashed T,Menon M,Thamilselvan S.Molecular mechanism of oxalate-induced free radical production and glutathione redox imbalance in renal epithelial cells:effect of antioxidants[J].Am J Nephrol,2004,24(5):557-568.

    [17]

    Hong S H,Lee H J,Sohn E J,et al.Anti-nephrolithic potential of resveratrol viainhibition of ROS,MCP-1,hyaluronan and osteopontin in vitro and in vivo[J].Pharmacol Rep,2013,65(4):970-979.

    [18]

    Tsujihata M.Mechanism of calcium oxalate renal stone formation andrenal tubular cell injury[J].Int J Urol,2008,15(2):115-120.

    [19]

    Cao L C,Honeyman T W,Cooney R,et al.Mitochondrial dysfunction isa primary event in renal cell oxalate toxicity[J].Kidney Int,2004,66(5):1890-1900.

    [20]

    Yu S L,Gan X G,Huang J M,et al.Oxalate impairs aminophospholipid translocase activity inrenal epithelial cells via oxidative stress:implications for calcium oxalateurolithiasis[J].J Urol,2011,186(3):1114-1120.

    [21]

    Abais J M,Xia M,Zhang Y,et al.Redox regulation of NLRP3 inflammasomes:ROS as trigger or effector[J].Antioxid Redox Signal,2015,22(13):1111-1129.

    [22]

    Feng H,Gu J,Gou F,et al.High Glucose and Lipopolysaccharide Prime NLRP3 Inflammasome via ROS/TXNIP Pathway in Mesangial Cells[J].J Diabetes Res,2016,2016:6973175.

    [23]

    Cao G,Jiang N,Hu Y,et al.Ruscogenin Attenuates Cerebral Ischemia-Induced Blood-Brain Barrier Dysfunction by Suppressing TXNIP/NLRP3 Inflammasome Activation and the MAPK Pathway[J].Int J Mol Sci,2016.

    [24]

    Xia M,Boini K M,Abais J M,et al.Endothelial NLRP3inflammasome activation and enhanced neointima formation in mice by adipokine visfatin[J].Am J Pathol,2014,184(5):1617-1628.

    [25]

    Mulay S R,Kulkarni O P,Rupanagudi K V,et al.Calcium oxalate crystals induce renal inflammation by NLRP3-mediated IL-1beta secretion[J].J Clin Invest,2013,123(1):236-246.

    [26]

    Kusmartsev S,Dominguez-Gutierrez P R,Canales B K,et al.Calcium Oxalate Stone Fragment and Crystal Phagocytosis by HumanMacrophages[J].J Urol,2016,195(4 Pt 1):1143-1151.

    [27]

    Ip W K E,Medzhitov R.Macrophages monitor tissue osmolarity and induce inflammatory response through NLRP3 and NLRC4 inflammasome activation[J].Nat Commun,2015,6:6931.

    [28]

    Bause A S,Matsui M S,Haigis M C.The protein deacetylase SIRT3 prevents oxidative stress-induced keratinocyte differentiation[J].J Biol Chem,2013,288(51):36484-36491.

    [29]

    Ferroni M C,Rycyna K J,Averch T D,et al.Vitamin D Repletion in Kidney Stone Formers-A Randomized Controlled Trial[J].J Urol,2017,197(4)1079-1083.

    [30]

    Wang L,Chen W,Peng Z,et al.Vorinostat protects against calcium oxalate-induced kidney injury in mice[J].Mol Med Rep,2015,12(3):4291-4297.

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收稿日期:  2018-07-17

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