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Int. J. Mol. Sci. 2017, 18(1), 174; doi:10.3390/ijms18010174

Glycative Stress and Its Defense Machinery Glyoxalase 1 in Renal Pathogenesis

1
Division of Nephrology and Endocrinology, The University of Tokyo Graduate School of Medicine, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
2
Division of Chronic Kidney Disease (CKD) Pathophysiology, The University of Tokyo Graduate School of Medicine, 7-3-1, Hongo, Bunkyo-ku, Tokyo 113-8655, Japan
*
Author to whom correspondence should be addressed.
Academic Editor: Casper G. Schalkwijk
Received: 9 December 2016 / Revised: 5 January 2017 / Accepted: 10 January 2017 / Published: 17 January 2017
(This article belongs to the Special Issue Glyoxalase System)
View Full-Text   |   Download PDF [470 KB, uploaded 17 January 2017]   |  

Abstract

Chronic kidney disease is a major public health problem around the world. Because the kidney plays a role in reducing glycative stress, renal dysfunction results in increased glycative stress. In turn, glycative stress, especially that due to advanced glycated end products (AGEs) and their precursors such as reactive carbonyl compounds, exacerbates chronic kidney disease and is related to premature aging in chronic kidney disease, whether caused by diabetes mellitus or otherwise. Factors which hinder a sufficient reduction in glycative stress include the inhibition of anti-glycation enzymes (e.g., GLO-1), as well as pathogenically activated endoplasmic reticulum (ER) stress and hypoxia in the kidney. Promising strategies aimed at halting the vicious cycle between chronic kidney disease and increases in glycative stress include the suppression of AGE accumulation in the body and the enhancement of GLO-1 to strengthen the host defense machinery against glycative stress. View Full-Text
Keywords: chronic kidney disease; AGEs; GLO-1; hypoxia; ER (Endoplasmic Reticulum) stress chronic kidney disease; AGEs; GLO-1; hypoxia; ER (Endoplasmic Reticulum) stress
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Hirakawa, Y.; Inagi, R. Glycative Stress and Its Defense Machinery Glyoxalase 1 in Renal Pathogenesis. Int. J. Mol. Sci. 2017, 18, 174.

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