[1]李雅,王志斌,刘玮晔,等.巨噬细胞与糖尿病肾病[J].国际内分泌代谢杂志,2014,(06):393-396.[doi:10.3760/cma.j.issn.1673-4157.2014.06.009]
　Li Ya*,Wang Zhibin,Liu Weiye,et al.Macrophages and diabetic nephropathy[J].International Journal of Endocrinology and Metabolism,2014,(06):393-396.[doi:10.3760/cma.j.issn.1673-4157.2014.06.009]
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巨噬细胞与糖尿病肾病()
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《国际内分泌代谢杂志》[ISSN:1673-4157/CN:12-1383/R]

卷:
期数:
2014年06期
页码:
393-396
栏目:
综述
出版日期:
2014-12-20

文章信息/Info

Title:
Macrophages and diabetic nephropathy
作者:
李雅; 王志斌; 刘玮晔; 仝令畅; 李玲; 张立超
750000 银川,宁夏医科大学药学院(李雅); 200433 上海,第二军医大学药学院药理教研室(李雅,王志斌,刘玮晔,仝令畅,李玲); 200137 上海市第七人民医院(李雅,张立超)
Author(s):
Li Ya*;  Wang Zhibin;  Liu Weiye;  Tong Lingchang;  Li Ling;  Zhang Lichao.
*College of Pharmacy, Ningxia Medical University, Yinchuan 750000, China
关键词:
巨噬细胞;  糖尿病肾病;  炎症
Keywords:
Macrophages;  Diabetic nephropathy;  Inflammation
DOI:
10.3760/cma.j.issn.1673-4157.2014.06.009
摘要:
糖尿病肾病是一种慢性炎性疾病,而巨噬细胞是重要的炎性细胞,在糖尿病肾病的发生、发展中起重要作用。血液中的单核细胞在选择素、细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)、单核细胞趋化蛋白-1(MCP-1)及骨桥蛋白等细胞黏附分子或趋化因子作用下经历滚动、黏附、迁移等过程,浸润于肾组织而分化成巨噬细胞,体内持续高血糖等因素使其活化,释放转化生长因子-β(TGF-β)、肿瘤坏死因子-α(TNF-α)、白细胞介素(IL)-1、IL-6、IL-18等细胞因子,促进肾小球系膜细胞分泌细胞外基质及成纤维细胞增殖,引起系膜细胞外基质沉淀、肾小球硬化及间质纤维化等肾损伤,从而促进糖尿病肾病的发展。调控巨噬细胞的浸润与活化可能是防治糖尿病肾病的新途径。
Abstract:
Diabetic nephropathy is a chronic inflammatory disease while macrophages are the key inflammatory cells and play important roles in the development and progression of diabetic nephropathy. The adhesion molecules or chemotactic factors, such as selectins, intercellular cell adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemotactic protein-1, and oesteopontin, induce peripheral blood monocytes rolling, adhesion and migration to kidney. Then most of these monocytes differentiate into macrophages. Under the sustained hyperglycemia, the infiltrative macrophages are activated, and release some cytokines such as transforming growth factor-β, tumor necrosis factor-α, interleukin-1, interleukin-6 and interleukin-18. These cytokines lead to the deposition of mesangial extracellular matrix, glomerular sclerosis and interstitial fibrosis through promoting the secretion of extracellular matrix from glomerular mesangial cells and the proliferation of fibroblast. Thus, the development of diabetic nephropathy is promoted. Regulating the infiltration and activation of macrophages may provide a new therapeutic approach for diabetic nephropathy.

参考文献/References:

[1] Nguyen D,Ping F,Mu W, et al.Macrophage accumulation in human progressive diabetic nephropathy[J].Nephrology(Carlton),2006,11(3):226-231.
[2] You H,Gao T,Cooper TK, et al.Macrophages directly mediate diabetic renal injury[J].Am J Physiol Renal Physiol,2013,305(12):F1719-F1727.
[3] Navarro-González JF,Mora-Fernández C,Muros de Fuentes M, et al.Inflammatory molecules and pathways in the pathogenesis of diabetic nephropathy[J].Nat Rev Nephrol,2011,7(6):327-340.
[4] Wang F,Xing T,Wang N, et al.Clinical significance of plasma CD146 and P-selectin in patients with type 2 diabetic nephropathy[J].Cytokine,2012,57(1):127-129.
[5] Tang WH,Lin FH,Lee CH, et al.Cilostazol effectively attenuates deterioration of albuminuria in patients with type 2 diabetes: a randomized, placebo-controlled trial[J].Endocrine,2014,45(2):293-301.
[6] Nagao T,Okura T,Irita J, et al.Osteopontin plays a critical role in interstitial fibrosis but not glomerular sclerosis in diabetic nephropathy[J].Nephron Extra,2012,2(1):87-103.
[7] Wang JC,Zhao Y,Chen SJ, et al.AOPPs induce MCP-1 expression by increasing ROS-mediated activation of the NF-κB pathway in rat mesangial cells: inhibition by sesquiterpene lactones[J].Cell Physiol Biochem,2013,32(6):1867-1877.
[8] Sasai Y,Iwakawa K,Yanagida K, et al.Advanced glycation endproducts stimulate renal epithelial cells to release chemokines that recruit macrophages, leading to renal fibrosis[J].Biosci Biotechnol Biochem,2012,76(9):1741-1745.
[9] Seok SJ,Lee ES,Kim GT, et al.Blockade of CCL2/CCR2 signalling ameliorates diabetic nephropathy in db/db mice[J].Nephrol Dial Transplant,2013,28(7):1700-1710.
[10] Nicholas SB,Liu J,Kim J, et al.Critical role for osteopontin in diabetic nephropathy[J].Kidney Int,2010,77(7):588-600.
[11] Choi HK,Kim TH,Jhon GJ, et al.Reactive Oxygen species regulate M-CSF-induced monocyte/macrophage proliferation through SHP1 oxidation[J].Cell Signal,2011,23(10):1633-1639.
[12] Lim AK,Ma FY,Nikolic-Paterson DJ, et al.Antibody blockade of c-fms suppresses the progression of inflammation and injury in early diabetic nephropathy in obese db/db mice[J].Diabetologia, 2009,52(8):1669-1679.
[13] Watanabe T,Tomioka NH,Doshi M, et al.Macrophage migration inhibitory factor is a possible candidate for the induction of microalbuminuria in diabetic db/db mice[J].Biol Pharm Bull,2013,36(5):741-747.
[14] Forbes JM,Coughlan MT,Cooper ME.Oxidative stress as a major culprit in kidney disease in diabetes[J].Diabetes,2008,57(6):1446-1454.
[15] Wang Z,Wei M,Wang M, et al.Inhibition of macrophage migration inhibitory factor reduces diabetic nephropathy in type Ⅱ diabetes mice[J].Inflammation,2014,37(3):847-858.
[16] Nagase R,Kajitani N,Shikata K, et al.Phenotypic change of macrophages in the progression of diabetic nephropathy; sialoadhesin-positive activated macrophages are increased in diabetic kidney[J].Clin Exp Nephrol,2012,16(5):739-748.
[17] Kamal F,Yanakieva-Georgieva N,Piao H, et al.Local delivery of angiotensinⅡ receptor blockers into the kidney passively attenuates inflammatory reactions during the early phases of streptozotocin-induced diabetic nephropathy through inhibition of calpain activity[J].Nephron Exp Nephrol,2010,115(3):e69-e79.
[18] Fernández-Real JM,Vendrell J,García I, et al.Structural damage in diabetic nephropathy is associated with TNF-α system activity[J].Acta Diabetol,2012,49(4):301-305.
[19] Gilbert RE,Zhang Y,Williams SJ, et al.A purpose-synthesised anti-fibrotic agent attenuates experimental kidney diseases in the rat[J].PLoS One,2012,7(10):e47160.
[20] Ota T,Takamura T,Ando H, et al.Preventive effect of cerivastatin on diabetic nephropathy through suppression of glomerular macrophage recruitment in a rat model[J].Diabetologia,2003,46(6):843-851.
[21] Shelbaya S,Amer H,Seddik S, et al.Study of the role of interleukin-6 and highly sensitive C-reactive protein in diabetic nephropathy in type 1 diabetic patients[J].Eur Rev Med Pharmacol Sci,2012,16(2):176-182.

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备注/Memo

备注/Memo:
基金项目:国家自然科学基金资助项目(81402941)
更新日期/Last Update: 2014-12-20