Inhibition of Calcium<sup>2+</sup>/Calmodulin-dependent Protein Kinase Type IV Ameliorates Experimental Nephrotic Syndrome-Reference-Cited by-同舟云学术

Inhibition of Calcium²⁺/Calmodulin-dependent Protein Kinase Type IV Ameliorates Experimental Nephrotic Syndrome

Published:2013 Issue:10 Volume:52 Page:1035-1041
ISSN:0918-2918
Container-title:Internal Medicine
language:en
Short-container-title:Intern. Med.

Author:

Ao Qiangguo¹,Cheng Qingli¹,Ma Qiang¹,Wang Xiaodan¹,Liu Sheng¹

Affiliation:

1. Department of Geriatric Nephrology, Institute of Gerontology, Chinese PLA General Hospital, China

Publisher

Japanese Society of Internal Medicine

Subject

General Medicine,Internal Medicine

Link

https://www.jstage.jst.go.jp/article/internalmedicine/52/10/52_52.9574/_pdf

Reference15 articles.

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2. 2. Reiser J, von Gersdorff G, Loos M, et al. Induction of B7-1 in podocytes is associated with nephrotic syndrome. J Clin Invest 113: 1390-1397, 2004.

3. 3. Kriz W, Gretz N, Lemley KV. Progression of glomerular diseases: is the podocyte the culprit? Kidney Int 54: 687-697, 1998.

4. 4. Ichinose K, Rauen T, Juang YT, et al. Cutting edge: Calcium/Calmodulin-dependent protein kinase type IV is essential for mesangial cell proliferation and lupus nephritis. J Immunol 187: 5500-5504, 2011.

5. 5. Ichinose K, Juang YT, Crispín JC, Kis-Toth K, Tsokos GC. Suppression of autoimmunity and organ pathology in lupus-prone mice upon inhibition of calcium/calmodulin-dependent protein kinase type IV. Arthritis Rheum 63: 523-529, 2011.

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