2015, Número 3
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Rev Cuba Endoc 2015; 26 (3)
Mecanismos de inducción de la matriz extracelular en la nefropatía diabética
Guzmán-Hernández EA, Segura-Cobos D
Idioma: Español
Referencias bibliográficas: 33
Paginas: 278-291
Archivo PDF: 225.69 Kb.
RESUMEN
La nefropatía diabética es una complicación grave en la diabetes mellitus. Sus
principales cambios morfológicos típicos se deben al aumento de la cantidad de
proteínas de la matriz extracelular. Los productos finales de glicación avanzada,
resultado de la hiperglucemia, estimulan la producción de proteínas de la matriz
extracelular en las células mesangiales, lo que resulta en la glomeruloesclerosis. Se
revisan las alteraciones de las vías metabólicas que inducen la producción de
factores que aumentan la síntesis de proteínas de la matriz extracelular y su
acumulación durante el desarrollo de la nefropatía diabética. La glucosa intracelular
elevada induce un aumento de angiotensina II y activación de proteína cinasa C,
que a su vez, aumentan varios factores de crecimiento, como el transformante 1, el
endotelial vascular, el de tejido conectivo, el epidérmico y el derivado de plaquetas,
que llevan al incremento en la síntesis de proteínas de la matriz extracelular renal,
como el colágeno, la fibronectina, la entactina y la laminina, lo que engrosará las
membranas basales y expandirá progresivamente la matriz mesangial glomerular.
Las metaloproteinasas de la matriz, que modulan la cantidad de proteínas de la
matriz extracelular, son, a su vez, reguladas por los inhibidores tisulares de las
metaloproteinasas.
REFERENCIAS (EN ESTE ARTÍCULO)
Kolset SO, Reinholt FP, Jenssen T. Diabetic Nephropathy and Extracellular Matrix. J Histochem Cytochem. 2012;60(12):976-86.
Fioretto P, Mauer M. Histopathology of diabetic nephropathy. Semin Nephrol. 2007;27:195-207.
Wolf G, Ziyadeh FN. Cellular and molecular mechanisms of proteinuria in diabetic nephropathy. Nephron Physiol. 2007;106(2):26-31.
Kanwar YS, Sun L, Xie P, Liu FY, Chen S. A glimpse of various pathogenetic mechanisms of diabetic nephropathy. Annu Rev Pathol. 2011;6:395-423.
Mariappan MM. Signaling mechanisms in the regulation of renal matrix metabolism in diabetes. Exp Diabetes Res. 2012;2012:749812. Epub 2012 Feb 19.
Morrison CJ, Butler GS, Rodriguez D, Overall CM. Matrix metalloproteinase proteomics: substrates, targets, and therapy. Curr Opin Cell Biol. 2009;21:645-53.
Maris M, Ferreira GB, D'Hertog W, Cnop M, Waelkens E, Overbergh L, Mathieu C. High glucose induces dysfunction in insulin secretory cells by different pathways: a proteomic approach. J Proteome Res. 2010;9(12):6274-87.
Flamment M, Foufelle F. Endoplasmic reticulum stress: from physiology to pathogenesis of type 2 diabetes. MedSci (Paris). 2013;29(8-9):756-64.
Wu Y, Tang L, Chen B. Oxidative Stress: Implications for the Development of Diabetic Retinopathy and Antioxidant Therapeutic Perspectives. Oxid Med Cell Longev. 2014;2014:1-12.
Ott C, Jacobs K, Haucke E, Navarrete Santos A, Grune T, Simm A. Role of advanced glycation end products in cellular signaling. Redox Biol. 2014;2:411-29.
Singh VP, Bali A, Singh N, Jaggi AS. Advanced Glycation End Products and Diabetic Complications. Korean J Physiol Pharmacol. 2014;18(1):1-14.
Schalkwijk CG, Miyata T. Early-and advanced non-enzymatic glycation in diabetic vascular complications: the search for therapeutics. Amino Acids. 2012;42(4):1193-204.
Manigrasso MB, Juranek J, Ramasamy R, Schmidt AM. Unlocking the Biology of RAGE in Diabetic Microvascular Complications. Trends Endocrinol Metab. 2014;25(1):10.
Chiu CJ, Taylor A. Dietary hyperglycemia, glycemic index and metabolic retinal diseases. Prog Retin Eye Res. 2011;30(1):18-53.
Maccari R, Ottanà R. Targeting aldose reductase for the treatment of diabetes complications and inflammatory diseases: new insights and future directions. J Med Chem. 2015;58(5):2047-67.
Kitada M, Zhang Z, Mima A, King GL. Molecular mechanisms of diabetic vascular complications. J Diabetes Investig. 2010;1(3):77-89.
Thallas-Bonke V, Cooper ME. Tandem Inhibition of PKC in Diabetic Nephropathy: It Takes Two to Tango? Diabetes. 2013;62(4):1010-11.
Heilig CW, Deb DK, Abdul A, Riaz H, James LR, Salameh J, Nahman NS Jr. GLUT1 regulation of the pro-sclerotic mediators of diabetic nephropathy. Am J Nephrol. 2013;38(1):39-49.
Mima A, Matsubara T, Arai H, Abe H, Nagai K, Kanamori H, et al. Angiotensin II-dependent Src and Smad1 signaling pathway is crucial for the development of diabetic nephropathy. Lab Invest. 2006;86:927-39.
Kumar PA, Brosius FC 3rd, Menon RK. The glomerular podocyte as a target of growth hormone action: implications for the pathogenesis of diabetic nephropathy. Curr Diabetes Rev. 2011;7(1):50-5.
Lan HY, Chung AC. TGF-β/Smad signaling in kidney disease. Semin Nephrol. 2012;32(3):236-43.
Kanwar YS, Sun L, Xie P, Liu FY, Chen S. A glimpse of various pathogenetic mechanisms of diabetic nephropathy. Annu Rev Pathol. 2011;6:395-423.
McLennan SV, Abdollahi M, Twigg SM. Connective tissue growth factor, matrix regulation, and diabetic kidney disease. Curr Opin Nephrol Hypertens. 2013;22(1):85-92.
Garud MS, Kulkarni YA. Hyperglycemia to nephropathy via transforming growth factor beta. Curr Diabetes Rev. 2014;10(3):182-9.
McLennan SV, Abdollahi M, Twigg SM. Connective tissue growth factor matrix regulation and diabetic kidney disease. Curr Opin Nephrol Hypertens. 2013;22:85-92.
Advani A. Vascular endothelial growth factor and the kidney: something of the marvellous. Curr Opin Nephrol Hypertens. 2014;23(1):87-92.
Tufro A,Veron D. VEGF and podocytes in diabetic nephropathy. Semin Nephrol. 2012;32(4):385-93.
Advani A, Wiggins KJ, Cox AJ, Zhang Y, Gilbert RE, Kelly DJ. Inhibition of the epidermal growth factor receptor preserves podocytes and attenuates albuminuria in experimental diabetic nephropathy. Nephrology. 2011;16(6):573-81.
Taniguchi K, Xia L, Goldberg HJ, Lee KW, Shah A, Stavar L, et al. Inhibition of Src kinase blocks high glucose-induced EGFR transactivation and collagen synthesis in mesangial cells and prevents diabetic nephropathy in mice. Diabetes. 2013;62(11):3874-86.
Wu O, Peng F, Zhang B, Ingram AJ, Gao B, Krepinsky JC. Collagen I induction by high glucose levels is mediated by epidermal growth factor receptor and phosphoinositide 3-kinase/Akt signaling in mesangial cells. Diabetologia. 2007;50(9):2008-18.
Boor P, Ostendorf T, Floege J. PDGF and the progression of renal disease. Nephrol Dial Transplant. 2014;29:i45–i54.
García PM, Getino MA, Domínguez V, Navarro JN. Inflammation in diabetic kidney disease. World J Diabetes. 2014;5(4):431-43.
Li SY, Huang PH, Yang AH, Tarng DC, Yang WC, Lin CC, et al. Matrix metalloproteinase-9 deficiency attenuates diabetic nephropathy by modulation of podocyte functions and dedifferentiation. Kidney Int. 2014;86(2):358-69.