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RISS 인기검색어
- 검색키워드
- 저자 : Shinji Kume (검색결과 3 건)
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Autophagy: A Novel Therapeutic Target for Diabetic Nephropathy
Shinji Kume,Daisuke Koya 대한당뇨병학회 2015 Diabetes and Metabolism Journal Vol.39 No.6
Diabetic nephropathy is a leading cause of end stage renal disease and its occurance is increasing worldwide. The most effective treatment strategy for the condition is intensive treatment to strictly control glycemia and blood pressure using renin-angiotensin system inhibitors. However, a fraction of patients still go on to reach end stage renal disease even under such intensive care. New therapeutic targets for diabetic nephropathy are, therefore, urgently needed. Autophagy is a major catabolic pathway by which mammalian cells degrade macromolecules and organelles to maintain intracellular homeostasis. The accumulation of damaged proteins and organelles is associated with the pathogenesis of diabetic nephropathy. Autophagy in the kidney is activated under some stress conditions, such as oxidative stress and hypoxia in proximal tubular cells, and occurs even under normal conditions in podocytes. These and other accumulating findings have led to a hypothesis that autophagy is involved in the pathogenesis of diabetic nephropathy. Here, we review recent findings underpinning this hypothesis and discuss the advantages of targeting autophagy for the treatment of diabetic nephropathy.
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Anti-aging molecule, Sirt1: a novel therapeutic target for diabetic nephropathy
Shinji Kume,Munehiro Kitada,Keizo Kanasaki,Hiroshi Maegawa,Daisuke Koya 대한약학회 2013 Archives of Pharmacal Research Vol.36 No.2
Caloric restriction prolongs the lifespan ofmany species. Therefore, investigators have researched theusefulness of caloric restriction for healthy lifespan extension. Sirt1, an NAD?-dependent deacetylase, was identifiedas a molecule necessary for caloric restriction-related antiagingstrategies. Sirt1 functions as an intracellular energysensor to detect the concentration of NAD?, and controlsin vivo metabolic changes under caloric restriction andstarvation through its deacetylase activity to many targetsincluding histones, nuclear transcriptional factors, andenzymes. During the past decade, investigators havereported the relationship between disturbance of Sirt1activation and the onset of aging- and obesity-associateddiseases such as diabetes, cardiovascular disease and neurodegenerativedisorders. Consequently, a calorie restriction-mimetic action of Sirt1 is now expected as a newtherapy for these diseases. In addition, recent studies havegradually clarified the role of Sirt1 in the onset of kidneydisease. Its activation may also become a new target oftreatment in the patients with chronic kidney diseaseincluding diabetic nephropathy. In this article, we wouldlike to review the role of Sirt1 in the onset of kidney diseasebased on previous studies, and discuss its possibility as thetarget of treatment in diabetic nephropathy.
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Ohashi, Natsuko,Morino, Katsutaro,Ida, Shogo,Sekine, Osamu,Lemecha, Mengistu,Kume, Shinji,Park, Shi-Young,Choi, Cheol Soo,Ugi, Satoshi,Maegawa, Hiroshi American Diabetes Association 2017 Diabetes Vol. No.
<P>Adipose tissues considerably influence metabolic homeostasis, and both white (WAT) and brown (BAT) adipose tissue play significant roles in lipid and glucose metabolism. O-linked N-acetylglucosamine (O-GlcNAc) modification is characterized by the addition of N-acetylglucosamine to various proteins by O-GlcNAc transferase (Ogt), subsequently modulating various cellular processes. However, little is known about the role of O-GlcNAc modification in adipose tissues. Here, we report the critical role of O-GlcNAc modification in cold-induced thermogenesis. Deletion of Ogt in WAT and BAT using adiponectin promoterdriven Cre recombinase resulted in severe cold intolerance with decreased uncoupling protein 1 (Ucp1) expression. Furthermore, Ogt deletion led to decreased mitochondrial protein expression in conjunction with decreased peroxisome proliferator-activated receptor gamma coactivator 1-alpha protein expression. This phenotype was further confirmed by deletion of Ogt in BAT using Ucp1 promoter-driven Cre recombinase, suggesting that O-GlcNAc modification in BAT is responsible for cold-induced thermogenesis. Hypothermia was significant under fasting conditions. This effect was mitigated after normal diet consumption but not after consumption of a fatty acid-rich ketogenic diet lacking carbohydrates, suggesting impaired diet-induced thermogenesis, particularly by fat. In conclusion, O-GlcNAc modification is essential for cold-induced thermogenesis and mitochondrial biogenesis in BAT. Glucose flux into BAT may be a signal to maintain BAT physiological responses.</P>
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