11β-Hydroxysteroid Dehydrogenase and the Syndrome of Apparent Mineralocorticoid Excess
11β-Hydroxysteroid Dehydrogenase and the Syndrome of Apparent Mineralocorticoid Excess
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DOI:
10.1210/edrv.18.1.0288
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发表时间:
1997-02
影响因子:
20.3
通讯作者:
P. White;T. Mune;T. Mune;Anil K. Agarwal
中科院分区:
文献类型:
--
作者:
P. White;T. Mune;T. Mune;Anil K. Agarwal
I. Introduction II. Biochemistry of Cortisol Metabolism III. Mineralocorticoid Receptor Function A. Actions of aldosterone B. Structure and function of the mineralocorticoid receptor C. Hypothesis: 11-HSD protects the mineralocorticoid receptor IV. Loss of Function of 11-HSD A. Syndrome of apparent mineralocorticoid excess (AME) B. Licorice intoxication C. Ectopic ACTH syndrome D. Essential hypertension E. Related conditions V. Functional Roles of 11-HSD A. Liver B. Kidney and other mineralocorticoid target tissues C. Brain D. Circulatory system E. Skin F. Ovary G. Placenta H. Other fetal tissues VI. The Type I (Liver) Isozyme of 11-HSD A. Terminology B. Biochemistry C. Molecular biology D. Expression E. Lack of involvement in the syndromes of AME or 11-reductase deficiency VII. The Type 2 (Kidney) Isozyme of 11-HSD A. Biochemistry B. Molecular biology C. Expression D. Mutations in HSD11B2 are detected in all patients with AME VIII. Summary\.