МЕХАНІЗМИ ПОРУШЕНЬ ФУНКЦІОНАЛЬНОГО ТА МОРФОЛОГІЧНОГО СТАНУ НИРОК ПРИ ЦУКРОВОМУ ДІАБЕТІ

Автор(и)

  • V. P. Gavaleshko ВДНЗ України «Буковинський державний медичний університет», м. Чернівці

DOI:

https://doi.org/10.24061/1727-4338.XIV.4.54.2015.45

Ключові слова:

цукровий діабет, нирки, морфофункціональний стан

Анотація

Узагальнено сучасні дані щодо патогенезу порушень морфофункціонального стану нирок при цукровому діабеті.

Посилання

Shestakova MV, Chugunova LA, Shamhalova MSh, Dedov II. Diabeticheskaja nefropatija: dostizhenija v diagnostike, profilaktike i lechenii [Diabetic Nephropathy: Advances in Diagnosis, Prevention and Treatment]. Saharnyj diabet. 2005;3:22-5. (in Russian).

McFarlane SI, McCullough PA, Sowers JR, et al. Сomparison of the CKD epidemiology collaboration (C KD-EPI) and modification of diet in renal disease (MDRD) study equations: prevalence of and risk Factors for Diabetes Mellitu s in CKD in the Kidney Early Evaluation Program (KEEP). Am. J. Kidney Dis. 2011;57(3 Suppl. 2):24-31.

Ballantyne СM. Adolescent type 1 Diabetes cardio-renal Intervention Trial (AdDIT). BMC Pediatr. 2009;9(1):79-86.

Rashidi A, Sehgal AR, Rahman M, O'Connor AS. The case for chronic kidney disease, diabetes mellitus, and myocardial infarction being equivalent risk factors for cardiovascular mortality in patients older than 65 years. Am. J. Cardiol. 2008;102(12):1668-73.

Kanda T, Wakino S, Hayashi K, Plutzky J. Cardiovascular Disease, Chronic Kidney Disease, and Type 2 Diabetes Mellitus: Proceeding with Caution at a Dangerous Intersection. J. Am. Soc. Nephrol. 2008;19(1):4-7.

Kantharidis P, Wang Bo, Carew RM, Lan H-Y. Diabetes Complications: The MicroRNA Perspective. Diabetes. 2011;60(7):1832-37.

Loboda OM, Dudar IO. Mekhanizmy rozvytku ta prohresuvannia diabetychnoi nefropatii [Mechanisms of development and progression of of diabetic nephropathy]. Klinichna imunolohiia, alerholohiia, infektolohiia. 2010;(9-10):46-50. (in Ukrainian).

Vidigal FC, Cocate PG, Pereira LG, Alfenas RCG. The role of hyperglycemia in the induction of oxidative stress and inflammatory process. Nutr. Hosp. 2012;27(5):1391-98.

Brouwers O, Niessen PM, Ferreira I, et al. Overexpression of glyoxalase-I reduces hyperglycemia-induced levels of advanced glycation end products and oxidative stress in diabetic rats. J. Biol. Chem. 2011;286(2):1374-80.

Shao D, Liu J, Ni J, et al. Suppression of XBP1S Mediates High Glucose-Induced Oxidative Stress and Extracellular Matrix Synthesis in Renal Mesangial Cell and Kidney of Diabetic Rats. PLoS One. 2013;8(2):56124.

Yao D, Brownlee M. Hyperglycemia-induced reactive oxygen species increase expression of the receptor for advanced glycation end products (RAGE) and RAGE ligands. Diabetes. 2010;59(1):249-55.

Nagai R, Murray DB, Metz TO. Chelation: a fundamental mechanism of action of AGE inhibitors, AGE breakers, and other inhibitors of diabetes complications. Diabetes. 2012;61(3):549-59.

Sangle GV, Zhao R, Mizuno TM, Shen GX. Involvement of RAGE, NADPH oxidase, and Ras/Raf-1 pathway in glycated LDL-induced expression of heat shock factor-1 and plasminogen activator inhibitor-1 in vascular endothelial cells. Endocrinology. 2010;151(9):4455–66.

Boghdady NA, Bard GA. Evaluation of oxidative stress markers and vascular risk factors in patients with diabetic peripheral neuropathy. Cell. Biochem. Funct. 2012;30(4):328–34.

Selvin E, Steffes MW, Zhu H, et al. Glycated hemoglobin, diabetes, and cardiovascular risk in nondiabetic adults. N. Engl. J. Med. 2010;362(9):800-11.

Eriksson M, Carlberg B, Eliasson M. The disparity in long-term survival after a first stroke in patients with and without diabetes persists: the Northern Sweden MONICA study. Cerebrovasc. Dis. 2012;34(2):153-60.

Laing SP, Swerdlow AJ, Slater SD, et al. Mortality from heart disease in a cohort of 23,000 patients with insulin-treated diabetes. Diabetologia. 2003;46(6):760-65.

Chung AC, Lan HY. Chemokines in renal injury. J. Am. Soc. Nephrol. 2011;22(5):802-09.

Duffield JS. Macrophages and immunologic inflammation of the kidney. Semin. Nephrol. 2010;30(3):234-54.

Olukman M, Orhan CE, Çelenk FG, Ülker S. Apocynin restores endothelial dysfunction in streptozotocin diabetic rats through regulation of nitric oxide synthase and NADPH oxidase expressions. J. Diabet. Complicat. 2010;24(6):415-23.

Raphael J, Gozal Y, Navot N, Zuo ZJ. Hyperglycemia inhibits anesthetic-induced postconditioning in the rabbit heart via modulation of phosphatidylinositol-3-kinase/Akt and endothelial nitric oxide synthase signaling. Cardiovasc. Pharmacol. 2010;55(4):348-57.

Grossin N, Wautier MP, Meas T. , et al. Severity of diabetic microvascular complications is associated with a low soluble RAGE level. Diabetes Metab. 2008;34(4 Pt1):392-95.

Yan SF, Ramasamy R, Schmidt AM. The RAGE axis: a fundamental mechanism signaling danger to the vulnerable vasculature. Circ. Res. 2010;106(5):842-53.

Ramasamy R, Yan SF, Schmidt AM. Receptor for AGE (RAGE): signaling mechanisms in the pathogenesis of diabetes and its complications. Ann. N. Y. Acad. Sci. 2011;1243:88-102.

Driianska VIe, Drannik HM, Marinenko MI, ta in. Faktory mizhklitynnoi kooperatsii imunnoi systemy (tsytokiny ta VCAM-1) u khvorykh na khronichnu khvorobu nyrok I-III stadii, diabetychnu nefropatiiu [Factors intercellular cooperation of the immune system (cytokines and VCAM-1) in patients with chronic kidney disease and third stages, diabetic nephropathy]. Imunolohiia ta alerholohiia: nauka i praktyka. 2010;1:95-8. (in Ukrainian).

Topchij II. Rol' ingibitora aktivatora plazminogena-1 v razvitii fibrozirujushhih processov v pochkah pri saharnom diabete II tipa [The role of the inhibitor of plasminogen-1 activator in the development of fibrotic processes in the kidneys in type II diabetes mellitus]. Ukrains'kyi terapevtychnyi zhurnal. 2010;1:42-8. (in Russian).

Lan HY. Diverse roles of TGF-beta/Smads in renal fibrosis and inflammation. Int. J. Biol. Sci. 2011;7(7):1056-67.

Fukami K, Ueda S, Yamagishi S, et al. AGEs activate mesangial TGF-beta-Smad signaling via an angiotensin II type I receptor interaction. Kidney Int. 2004;66(6):2137-47.

Hopfer U, Hopfer H, Meyer-Schwesinger C, et al. Lack of type VIII collagen in mice ameliorates diabetic nephropathy. Diabetes. 2009;58(7):1672–81.

Loeffler I, Hopfer U, Koczan D, Wolf G J. Type VIII collagen modulates TGF-β1-induced proliferation of mesangial cells. Am. Soc. Nephrol. 2011;22(4):649-63.

Nosadini R, Tonolo G. Role of oxidized low density lipoproteins and free fatty acids in the pathogenesis of glomerulopathy and tubulointerstitial lesions in type 2 diabetes. Nutr. Metab. Cardiovasc. Dis. 2011;21(2):79-85.

Barnes JL, Gorin Y. Myofibroblast differentiation during fibrosis: role of NAD(P)H oxidases. Kidney Int. 2011;79(9):944-56.

Huh KH, Ahn HJ, Park J, et al. Mycophenolic acid inhibits oleic acid-induced mesangial cell activation through both cellular reactive oxygen species and inosine monophosphate dehydrogenase 2 pathways. Pediatr. Nephrol. 2009;24(4):737-45.

Nakhjavani M, Esteghamati A, Khalilzadeh O, et al. Association of mіcroalbuminuria with oxidized LDL and TGF-beta in type 2 diabetic patients: a case-control study. Int. Urol. Nephrol. 2010;42(2):487-92.

Elsner M, Gehrmann W, Lenzen S. Peroxisome-generated hydrogen peroxide as important mediator of lipotoxicity in insulin-producing cells. Diabetes. 2011;60(1):200-08.

Fransen M, Nordgren M, Wang B, Apanasets О. Role of peroxisomes in ROS/RNS-metabolism: implications for human disease. Biochim. Biophys. Acta. 2012;1822(9):1363-73.

Ivashchenko O, Van Veldhoven PP, Brees C, et al. Intraperoxisomal redox balance in mammalian cells: oxidative stress and interorganellar cross-talk. Mol. Biol. Cell. 2011;22(9):1440-51.

Lezhenko HO, Pashkova OIe, Kamenshchyk AV, ta in. Otsinka roli transformuiuchoho faktoru rostu-beta u formuvanni diabetychnoi nefropatii u ditei, khvorykh na tsukrovyi diabet [Evaluation of the role of transforming growth factor-beta in the formation diabetychnoyi nefropatiyi in children with diabetes mellitus]. Problemy endokrynnoi patolohii. 2010;1:56-61. (in Ukrainian).

Gorin Y, Block K, Hernandez J. J, et al. Nox4 NAD(P)H oxidase mediates hypertrophy and fibronectin expression in the diabetic kidney. J. Biol. Chem. 2005;280(47):39616-26.

Eid AA, Lee DY, Roman LJ, et al. Sestrin 2 and AMPK connect hyperglycemia to Nox4-dependent eNOS uncoupling and matrix protein expression. Mol. Cell. Biol. 2013;33(17):23439-60.

Liu Y. Cellular and molecular mechanisms of renal fibrosis. Nat. Rev. Nephrol. 2011;7(12):684-96.

Sedeek M, Callera G, Montezano A, et al. Critical role of Nox4-based NADPH oxidase in glucose-induced oxidative stress in the kidney: implications in type 2 diabetic nephropathy. Am. J. Physiol. Renal Physiol. 2010;299(6):1348-58.

Park J, Kwon MK, Huh JY, et al. Renoprotective antioxidant effect of alagebrium in experimental diabetes. Nephrol. Dial. Transplant. 2011;26(11):3474-84.

Sedeek M, Gutsol A, Montezano AC. Renoprotective effects of a novel Nox1/4 inhibitor in a mouse model of Type 2 diabetes. Clin. Sci. 2013;124(3):191-202.

Pchelin IJu, Shishkina AN, Lapteva OA. Rol' sistemnogo i lokal'nogo vospalenija v razvitii diabeticheskoj nefropatii [The role of systemic and local inflammation in the development of diabetic nephropathy]. Nefrologija. 2011;15(4):21-6. (in Russian).

Zhang M, Gao X, Wu J, et al. Oxidized high-density lipoprotein enhances inflammatory activity in rat mesangial cells. Diabetes Metab. Res. Rev. 2010;26(6):455-63.

Wada J, Makino H. Inflammation and the pathogenesis of diabetic nephropathy. Clin. Sci. 2013;124(3):139-52.

Cortes-Rojo C, Calderon-Cortes E, Clemente-Guerrero M, et al. Elucidation of the effects of lipoperoxidation on the mitochondrial electron transport chain using yeast mitochondria with manipulated fatty acid content. J. Bioenerg. Biomembr. 2009;41(1):15-28.

Mankovskyi BM, Malynovska OV. Vplyv hipolipidemichnoi terapii symvastatynom na mikroal'buminuriiu u khvorykh na tsukrovyi diabet [Effect of simvastatin on lipid-lowering therapy microalbuminuria in patients with diabetes]. Sertse i sudyny. 2010;1:41-5. (in Ukrainian).

Rivero C, Mora M, Muros J, et al. Pathogenic perspectives for the role of inflammation in diabetic nephropathy. Clin. Sci. 2009;116(6):479-92.

Navarro-González JF, Mora-Fernández C, De Fuentes MM, García-Pérez J. Inflammatory molecules and pathways in the pathogenesis of diabetic nephropathy. Nat. Rev. Nephrol. 2011;7(6):327-40.

Mima A. Inflammation and Oxidative Stress in Diabetic Nephropathy: New Insights on Its Inhibition as New Therapeutic Targets [Internet]. Journal of Diabetes Research Volume. 2013. Article ID 248563, 8 pages. URL: http://dx.doi.org/10.1155/2013/248563

Moreno JA, Izquierdo MC, Sanchez-Nino MD, et al. The inflammatory cytokines TWEAK and TNFα reduce renal klotho expression through NFκB. J. Am. Soc. Nephrol. 2011;22(7):1315-25.

Wu C-C, Chen J-S, Lu K-C, et al. Aberrant cytokines/chemokines production correlate with proteinuria in patients with overt diabetic nephropathy. Clin. Chim. Acta. 2010;411(9-10):700-04.

Mima A, Hiraoka-Yamomoto J, Li Q, et al. Protective effects of GLP-1 on glomerular endothelium and its inhibition by PKCbeta activation in diabetes. Diabetes. 2012;61(12):2967-79.

Cheng A, Dong Y, Zhu F, et al. AGE-LDL activates Toll like receptor 4 pathway and promotes inflammatory cytokines production in renal tubular epithelial cells. J. Int. J. Biol. Sci. 2013;9(1):94-107.

Zieman SJ, Melenovsky V, Clattenburg L, et al. Advanced glycation endproduct crosslink breaker (alagebrium) improves endothelial function in patients with isolated systolic hypertension. J. Hypertens. 2007;25(3):577-83.

Hartog JW, Willemsen S, van Veldhuisen DJ, et al. Effects of alagebrium, an advanced glycation endproduct breaker, on exercise tolerance and cardiac function in patients with chronic heart failure. Eur. J. Heart Fail. 2011;13(8):899-908.

Jauregui A, Mintz DH, Mundel P, Fornoni A. Role of altered insulin signaling pathways in the pathogenesis of podocyte malfunction and microalbuminuria. Curr. Opin. Nephrol. Hypertens. 2009;18(6):539-45.

Saltykov BB. Mehanizmy razvitija diabeticheskoj nefropatii [Mechanisms of development of diabetic nephropathy]. Arhiv patologii. 2008;70():38-42. (in Russian).

Nasrallah R, Robertson SJ, Hebert RL. Chronic COX inhibition reduces diabetes-induced hyperfiltration, proteinuria, and renal pathological markers in 36-week B6-Ins2(Akita) mice. Am. J. Nephrol. 2009;30(4):346-53.

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2017-04-07

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