Attenuation of Kidney Injuries Maintains Serum Sulfatide Levels Dependent on Hepatic Synthetic Ability: A Possible Involvement of Oxidative Stress-Reference-Cited by-同舟云学术

Attenuation of Kidney Injuries Maintains Serum Sulfatide Levels Dependent on Hepatic Synthetic Ability: A Possible Involvement of Oxidative Stress

Published:2012 Issue:1 Volume:227 Page:1-12
ISSN:0040-8727
Container-title:The Tohoku Journal of Experimental Medicine
language:en
Short-container-title:Tohoku J. Exp. Med.

Author:

Sheng Xiaona¹²,Nakajima Takero¹,Wang Lixuan¹³,Zhang Xiaowei¹⁴,Kamijo Yuji¹⁵,Takahashi Kyoko¹⁵,Tanaka Naoki¹,Sugiyama Eiko¹⁶,Kyogashima Mamoru⁷,Aoyama Toshifumi¹,Hara Atsushi¹

Affiliation:

1. Department of Metabolic Regulation, Institute on Aging and Adaptation, Shinshu University Graduate School of Medicine

2. Department of Neurology, The Second Hospital of Hebei Medical University

3. Department of Histology and Embryology, Hebei Medical University

4. Department of Neurosurgery, The Second Hospital of Hebei Medical University

5. Department of Nephrology, Shinshu University School of Medicine

6. Department of Nutritional Science, Nagano Prefectural College

7. Division of Microbiology and Molecular Cell Biology, Nihon Pharmaceutical University

Publisher

Tohoku University Medical Press

Subject

General Biochemistry, Genetics and Molecular Biology,General Medicine

Link

https://www.jstage.jst.go.jp/article/tjem/227/1/227_1_1/_pdf

Reference41 articles.

1. Cytochrome P-450 hPCN3, a Novel Cytochrome P-450 IIIA Gene Product That Is Differentially Expressed in Adult Human Liver

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3. Rat very-long-chain acyl-CoA dehydrogenase, a novel mitochondrial acyl-CoA dehydrogenase gene product, is a rate-limiting enzyme in long-chain fatty acid beta-oxidation system. cDNA and deduced amino acid sequence and distinct specificities of the cDNA-expressed protein.

4. Altered Constitutive Expression of Fatty Acid-metabolizing Enzymes in Mice Lacking the Peroxisome Proliferator-activated Receptor α (PPARα)

5. Bach1 inhibits oxidative stress–induced cellular senescence by impeding p53 function on chromatin

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