nach oben

Clinical and Experimental Nephrology

Erschienen in:

01.04.2014 | Review Article

Interventions against nutrient-sensing pathways represent an emerging new therapeutic approach for diabetic nephropathy

verfasst von: Daisuke Koya, Munehiro Kitada, Shinji Kume, Keizo Kanasaki

Erschienen in: Clinical and Experimental Nephrology | Ausgabe 2/2014

Einloggen, um Zugang zu erhalten

Abstract

Autophagy has evolved as a stress response that allows unicellular eukaryotic organisms to survive in starved conditions by regulating energy homeostasis and/or by protein and organelle quality control. The diabetes-induced accumulation of damaged proteins and organelles results in the development and progression of diabetic nephropathy. In contrast, autophagy machinery is activated by calorie restriction and environmental stress in proximal tubular cells, and is maintained at a high level in podocytes, suggesting its crucial role in the pathogenesis of diabetic nephropathy. However, its role in diabetic nephropathy has not been fully known. Here, we will discuss the role of autophagy and its involvement in the pathogenesis of diabetic nephropathy.

Abbate M, Zoja C, Remuzzi G. How does proteinuria cause progressive renal damage? J Am Soc Nephrol. 2006;17:2974–84.PubMedCrossRef

Forbes JM, Cooper ME. Mechanisms of diabetic complications. Physiol Rev. 2013;93:137–88.PubMedCrossRef

Kitada M, Zhang Z, Mima A, et al. Molecular mechanisms of diabetic vascular complications. J Diabetes Invest. 2010;1:77–89.CrossRef

Brownlee M. The pathobiology of diabetic complications: a unifying mechanism. Diabetes. 2005;54:1615–25.PubMedCrossRef

Dunlop M. Aldose reductase and the role of the polyol pathway in diabetic nephropathy. Kidney Int. 2000;Suppl 77:S3–12.CrossRef

Koya D, King GL. Protein kinase C activation and the development of diabetic complications. Diabetes. 1998;47:859–66.PubMedCrossRef

Forbes JM, Fukami K, Cooper ME. Diabetic nephropathy: where hemodynamics meets metabolism. Exp Clin Endocrinol Diabetes. 2007;115:69–84.PubMedCrossRef

Koya D, Araki S, Haneda M. Therapeutic management of diabetic kidney disease. J Diabetes Invest. 2011;2:248–54.CrossRef

Singh R, Kaushik S, Wang Y, et al. Autophagy regulates lipid metabolism. Nature. 2009;458:1131–5.PubMedCentralPubMedCrossRef

10.

Yoshizaki T, Kusunoki C, Kondo M, et al. Autophagy regulates inflammation in adipocytes. Biochem Biophys Res Commun. 2012;417:352–7.PubMedCrossRef

11.

Huber TB, Edelstein CL, Hartleben B, et al. Emerging role of autophagy in kidney function, diseases and aging. Autophagy. 2012;8:1009–31.PubMedCentralPubMedCrossRef

12.

Hartleben B, Godel M, Meyer-Schwesinger C, et al. Autophagy influences glomerular disease susceptibility and maintains podocyte homeostasis in aging mice. J Clin Invest. 2010;120:1084–96.PubMedCentralPubMedCrossRef

13.

Jiang M, Liu K, Luo J, et al. Autophagy is a renoprotective mechanism during in vitro hypoxia and in vivo ischemia-reperfusion injury. Am J Pathol. 2010;176:1181–92.PubMedCentralPubMedCrossRef

14.

Kume S, Uzu T, Horiike K, et al. Calorie restriction enhances cell adaptation to hypoxia through Sirt1-dependent mitochondrial autophagy in mouse aged kidney. J Clin Invest. 2010;120:1043–55.PubMedCentralPubMedCrossRef

15.

Liu S, Hartleben B, Kretz O, et al. Autophagy plays a critical role in kidney tubule maintenance, aging and ischemia-reperfusion injury. Autophagy. 2012;8:826–37.PubMedCrossRef

16.

Periyasamy-Thandavan S, Jiang M, Wei Q, et al. Autophagy is cytoprotective during cisplatin injury of renal proximal tubular cells. Kidney Int. 2008;74:631–40.PubMedCrossRef

17.

Takahashi A, Kimura T, Takabatake Y, et al. Autophagy guards against cisplatin-induced acute kidney injury. Am J Pathol. 2012;180:517–25.PubMedCrossRef

18.

Kume S, Thomas MC, Koya D. Nutrient sensing, autophagy, and diabetic nephropathy. Diabetes. 2012;61:23–9.PubMedCentralPubMedCrossRef

19.

Tanaka Y, Kume S, Kitada M, et al. Autophagy as a therapeutic target in diabetic nephropathy. Exp Diabetes Res. 2012;2012:628978.PubMedCentralPubMedCrossRef

20.

Lee CH, Inoki K, Guan KL. mTOR pathway as a target in tissue hypertrophy. Annu Rev Pharmacol Toxicol. 2007;47:443–67.PubMedCrossRef

21.

Chen JK, Chen J, Neilson EG, et al. Role of mammalian target of rapamycin signaling in compensatory renal hypertrophy. J Am Soc Nephrol. 2005;16:1384–91.PubMedCrossRef

22.

Sakaguchi M, Isono M, Isshiki K, et al. Inhibition of mTOR signaling with rapamycin attenuates renal hypertrophy in the early diabetic mice. Biochem Biophys Res Commun. 2006;340:296–301.PubMedCrossRef

23.

Yang Y, Wang J, Qin L, et al. Rapamycin prevents early steps of the development of diabetic nephropathy in rats. Am J Nephrol. 2007;27:495–502.PubMedCrossRef

24.

Sataranatarajan K, Mariappan MM, Lee MJ, et al. Regulation of elongation phase of mRNA translation in diabetic nephropathy: amelioration by rapamycin. Am J Pathol. 2007;171:1733–42.PubMedCentralPubMedCrossRef

25.

Mori H, Inoki K, Masutani K, et al. The mTOR pathway is highly activated in diabetic nephropathy and rapamycin has a strong therapeutic potential. Biochem Biophys Res Commun. 2009;384:471–5.PubMedCrossRef

26.

Godel M, Hartleben B, Herbach N, et al. Role of mTOR in podocyte function and diabetic nephropathy in humans and mice. J Clin Invest. 2011;121:2197–209.PubMedCentralPubMedCrossRef

27.

Inoki K, Mori H, Wang J, et al. mTORC1 activation in podocytes is a critical step in the development of diabetic nephropathy in mice. J Clin Invest. 2011;121:2181–96.PubMedCentralPubMedCrossRef

28.

Sarbassov DD, Ali SM, Sabatini DM. Growing roles for the mTOR pathway. Curr Opin Cell Biol. 2005;17:596–603.PubMedCrossRef

29.

Kroemer G, Marino G, Levine B. Autophagy and the integrated stress response. Mol Cell. 2010;40:280–93.PubMedCentralPubMedCrossRef

30.

Ravikumar B, Sarkar S, Davies JE. Regulation of mammalian autophagy in physiology and pathophysiology. Physiol Rev. 2010;90:1383–435.PubMedCrossRef

31.

Ding DF, You N, Wu XM, et al. Resveratrol attenuates renal hypertrophy in early-stage diabetes by activating AMPK. Am J Nephrol. 2010;31:363–74.PubMedCrossRef

32.

Fang L, Zhou Y, Cao H, et al. Autophagy attenuates diabetic glomerular damage through protection of hyperglycemis-induced podocyte injury. PLoS One. 2013;8:e60546.PubMedCentralPubMedCrossRef

33.

Cammisotto PG, Londono I, Gingras D, et al. Control of glycogen synthase through ADIPOR1-AMPK pathway in renal distal tubules of normal and diabetic rats. Am J Physiol Renal Physiol. 2008;294:F881–9.PubMedCrossRef

34.

Sokolovska J, Isajevs S, Sugoka O, et al. Influence of metformin on GLUT1 gene and protein expression in rat streptozotocin diabetes mellitus model. Arch Physiol Biochem. 2010;116:137–45.PubMedCrossRef

35.

Yamazaki T, Tanimoto M, Gohda T, et al. Combination effects of enalapril and losartan on lipid peroxidation in the kidneys of KK-Ay/Ta mice. Nephron Exp Nephrol. 2009;113:e66–76.PubMedCrossRef

36.

Chang CC, Chang CY, Wu YT, et al. Resveratrol retards progression of diabetic nephropathy through modulations of oxidative stress, proinflammatory cytokines, and AMP-activated protein kinase. J Biomed Sci. 2011;18:47.PubMedCentralPubMedCrossRef

37.

Lee MJ, Feliers D, Mariappan MM, et al. A role for AMP-activated protein kinase in diabetes-induced renal hypertrophy. Am J Physiol Renal Physiol. 2007;292:F617–27.PubMedCrossRef

38.

Kume S, Uzu T, Araki S, et al. Role of altered renal lipid metabolism in the development of renal injury induced by a high-fat diet. J Am Soc Nephrol. 2007;18:2715–23.PubMedCrossRef

39.

Tanaka Y, Kume S, Araki S, et al. Fenofibrate, a PPARalpha agonist, has renoprotective effects in mice by enhancing renal lipolysis. Kidney Int. 2011;79:871–82.PubMedCrossRef

40.

Jiang T, Wang Z, Proctor G, et al. Diet-induced obesity in C57BL/6J mice causes increased renal lipid accumulation and glomerulosclerosis via a sterol regulatory element-binding protein-1c-dependent pathway. J Biol Chem. 2005;280:32317–25.PubMedCrossRef

41.

Wang Z, Jiang T, Li J, et al. Regulation of renal lipid metabolism, lipid accumulation, and glomerulosclerosis in FVBdb/db mice with type 2 diabetes. Diabetes. 2005;54:2328–35.PubMedCrossRef

42.

Saha AK, Ruderman NB. Malonyl-CoA and AMP-activated protein kinase: an expanding partnership. Mol Cell Biochem. 2003;253:65–70.PubMedCrossRef

43.

Canto C, Auwerx J. AMP-activated protein kinase and its downstream transcriptional pathways. Cell Mol Life Sci. 2010;67:3407–23.PubMedCentralPubMedCrossRef

44.

Steinberg GR, Kemp BE. AMPK in health and disease. Physiol Rev. 2009;89:1025–78.PubMedCrossRef

45.

Lee JW, Park S, Takahashi Y, et al. The association of AMPK with ULK1 regulates autophagy. PLoS One. 2010;5:e15394.PubMedCentralPubMedCrossRef

46.

Behrends C, Sowa ME, Gygi SP, et al. Network organization of the human autophagy system. Nature. 2010;466:68–76.PubMedCentralPubMedCrossRef

47.

Kitada M, Kume S, Takeda-Watanabe A, et al. Sirtuins and renal diseases: relationship with aging and diabetic nephropathy. Clin Sci (Lond). 2013;124:153–64.CrossRef

48.

Kitada M, Kume S, Kanasaki K, et al. Sirtuins as possible drug targets in type 2 diabetes. Curr Drug Targets. 2013;14:622–36.PubMedCrossRef

49.

Liang F, Kume S, Koya D. SIRT1 and insulin resistance. Nat Rev Endocrinol. 2009;5:367–73.PubMedCrossRef

50.

Imai S, Guarente L. Ten years of NAD-dependent SIR2 family deacetylases: implications for metabolic diseases. Trends Pharmacol Sci. 2010;31:212–20.PubMedCentralPubMed

51.

Lee IH, Cao L, Mostoslavsky R, et al. A role for the NAD-dependent deacetylase Sirt1 in the regulation of autophagy. Proc Natl Acad Sci USA. 2008;105:3374–9.PubMedCentralPubMedCrossRef

52.

Canto C, Gerhart-Hines Z, Feige JN, et al. AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity. Nature. 2009;458:1056–60.PubMedCentralPubMedCrossRef

53.

Ghosh HS, McBurney M, Robbins PD. SIRT1 negatively regulates the mammalian target of rapamycin. PLoS One. 2010;5:e9199.PubMedCentralPubMedCrossRef

54.

Tikoo K, Tripathi DN, Kabra DG, et al. Intermittent fasting prevents the progression of type I diabetic nephropathy in rats and changes the expression of Sir2 and p53. FEBS Lett. 2007;581:1071–8.PubMedCrossRef

55.

Tikoo K, Singh K, Kabra D, et al. Change in histone H3 phosphorylation, MAP kinase p38, SIR 2 and p53 expression by resveratrol in preventing streptozotocin induced type I diabetic nephropathy. Free Radic Res. 2008;42:397–404.PubMedCrossRef

56.

Kitada M, Takeda A, Nagai T, et al. Dietary restriction ameliorates diabetic nephropathy through anti-inflammatory effects and regulation of the autophagy via restoration of Sirt1 in diabetic Wistar fatty (fa/fa) rats: a model of type 2 diabetes. Exp Diabetes Res. 2011;2011:908185.PubMedCentralPubMedCrossRef

Titel: Interventions against nutrient-sensing pathways represent an emerging new therapeutic approach for diabetic nephropathy
verfasst von: Daisuke Koya
Munehiro Kitada
Shinji Kume
Keizo Kanasaki
Publikationsdatum: 01.04.2014
Verlag: Springer Japan
Erschienen in: Clinical and Experimental Nephrology / Ausgabe 2/2014
Print ISSN: 1342-1751
Elektronische ISSN: 1437-7799
DOI: https://doi.org/10.1007/s10157-013-0908-3

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

^{Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag}

Kostenlos registrieren

Neu im Fachgebiet Innere Medizin

19.04.2024 | Vorhofflimmern | Nachrichten

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen

Live-Webinar: Aktuelle Leitlinien bei Herz-Kreislauf-Erkrankungen

Springer Medizin

Interventions against nutrient-sensing pathways represent an emerging new therapeutic approach for diabetic nephropathy

Abstract

Leitlinien kompakt für die Innere Medizin

Neu im Fachgebiet Innere Medizin

Parodontalbehandlung verbessert Prognose bei Katheterablation

Antihypertensiva schützen auch alte Menschen noch vor Demenz

Stereotaktische Radiatio schlägt konventionelle Bestrahlung

Denken Sie bei starker Blutung auch an die Hemmkörper-Hämophilie

Update Innere Medizin

Live-Webinar: Aktuelle Leitlinien bei Herz-Kreislauf-Erkrankungen

Springer Medizin

Abstract

Bitte loggen Sie sich ein, um Zugang zu diesem Inhalt zu erhalten

Weitere Artikel der Ausgabe 2/2014

Genetic associations in diabetic nephropathy

Role of dyslipidemia in impairment of energy metabolism, oxidative stress, inflammation and cardiovascular disease in chronic kidney disease

In vivo kinetic studies to further understand pathogenesis of abnormal lipoprotein metabolism in chronic kidney disease

Comparison between consecutive and intermittent steroid pulse therapy combined with tonsillectomy for clinical remission of IgA nephropathy

Abnormal lipoprotein metabolism in diabetic nephropathy

Results of the 4D study: ten years of follow-up?

Leitlinien kompakt für die Innere Medizin

Neu im Fachgebiet Innere Medizin

Parodontalbehandlung verbessert Prognose bei Katheterablation

Antihypertensiva schützen auch alte Menschen noch vor Demenz

Stereotaktische Radiatio schlägt konventionelle Bestrahlung

Denken Sie bei starker Blutung auch an die Hemmkörper-Hämophilie

Update Innere Medizin