The actin cytoskeleton of kidney podocytes is a direct target of the antiproteinuric effect of cyclosporine A

被引:0
作者
Christian Faul
Mary Donnelly
Sandra Merscher-Gomez
Yoon Hee Chang
Stefan Franz
Jacqueline Delfgaauw
Jer-Ming Chang
Hoon Young Choi
Kirk N Campbell
Kwanghee Kim
Jochen Reiser
Peter Mundel
机构
[1] University of Miami Miller School of Medicine,Department of Medicine
[2] Mount Sinai School of Medicine,Department of Medicine
[3] One Gustave L. Levy Place,Department of Internal Medicine
[4] Hsiao-Kang Municipal Hospital,Nephrology Division and Program in Glomerular Disease, Department of Medicine
[5] Kaohsiung,undefined
[6] Medical University,undefined
[7] Massachusetts General Hospital,undefined
[8] Harvard Medical School,undefined
[9] Present addresses: Department of Medicine,undefined
[10] Yale New Haven Hospital,undefined
[11] 20 York Street,undefined
[12] New Haven,undefined
[13] Connecticut 06510,undefined
[14] USA (Y.H.C.); Roche Pharma Switzerland,undefined
[15] Schönmattstrasse 2,undefined
[16] CH-4153 Reinach,undefined
[17] Switzerland (S.F.); Development Science,undefined
[18] Grünenthal,undefined
[19] Ziegelstrasse,undefined
[20] D-52078 Aachen,undefined
[21] Germany (J.D.).,undefined
来源
Nature Medicine | 2008年 / 14卷
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摘要
Currently, there are few options for treating chronic kidney disease. The immunosuppressant cyclosporine A is effective, but the mechanism has been unclear. In this new report, the authors now show that the benefit of cyclosporine A is not through an effect on the immune system but rather through stabilizing the cytoskeleton, and thus the integrity, of a key cell type needed for proper kidney function.
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页码:931 / 938
页数:7
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