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- 五十里 彰
- 静岡県立大学薬学部生体情報分子解析学
書誌事項
- タイトル別名
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- Molecular Physiological Study of Electrolyte Transporters in Renal Tubular Epithelial Cells
- ジンニョウ サイカン ジョウヒ サイボウ ニ オケル デンカイシツ ユソウタイ ノ ブンシ セイリガクテキ ケンキュウ
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Patients with lifestyle-related diseases such as hypertension, diabetes, and hyperlipidemia are at high risk for the pathogenesis of a life-threatening atherosclerotic disease. The elucidation of the mechanism responsible for the pathogenesis can bring about the prevention and the cure of lifestyle-related diseases. We think that abnormal transport of electrolytes in renal tubule is involved in lifestyle-related diseases and renal failure. This review focuses on the regulatory mechanisms of Mg2+ transport pathways in renal tubular cells. Mg2+ filtrated by glomeruli is reabsorbed by transcellular and paracellular pathways in renal epithelial cells. Transient receptor potential melastatin 6 (TRPM6) channel is expressed in the apical membrane and involved in the reabsorption of Mg2+. Cyclosporine A decreased TRPM6 expression and Mg2+ influx, suggesting that the decrease in TRPM6 expression may cause hypomagnesemia. Claudin-16 is expressed in the tight junction (TJ) of the thick ascending limb of Henle and may be involved in the paracellular Mg2+ transport. We found that the phosphorylation of claudin-16 is necessary for its localization on the TJ and claudin-16 is de-phosphorylated in Dahl salt-sensitive (DS) hypertensive rats. In epidemiologic studies, magnesium is the correlate of both systolic and diastolic blood pressure. Dysfunction of claudin-16 may be involved in the salt-sensitive hypertension. Dysfunction of Mg2+ reabsorption in renal tubule may be involved in renal failure and lifestyle-related diseases.<br>
収録刊行物
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- 薬学雑誌
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薬学雑誌 129 (9), 1025-1031, 2009-09-01
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390282681104024704
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- NII論文ID
- 130000135999
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- NII書誌ID
- AN00284903
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- ISSN
- 13475231
- 00316903
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- NDL書誌ID
- 10373778
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- 本文言語コード
- ja
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- データソース種別
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- JaLC
- NDL
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- 使用不可