11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) interconverts the inactive glucocorticoid cortisone and its active form cortisol. It is widely expressed and, although bidirectional, in vivo it functions predominantly as an oxoreductase, generating active glucocorticoid. This allows glucocorticoid receptor activation to be regulated at a prereceptor level in a tissue-specific manner. In this review, we will discuss the enzymology and molecular biology of 11β-HSD1 and the molecular basis of cortisone reductase deficiencies. We will also address how altered 11β-HSD1 activity has been implicated in a number of disease states, and we will explore its role in the physiology and pathologies of different tissues. Finally, we will address the current status of selective 11β-HSD1 inhibitors that are in development and being tested in phase II trials for patients with the metabolic syndrome. Although the data are preliminary, therapeutic inhibition of 11β-HSD1 is also an exciting prospect for the treatment of a variety of other disorders such as osteoporosis, glaucoma, intracranial hypertension, and cognitive decline.

中文翻译：

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11β-羟基类固醇脱氢酶 1：转化和治疗方面。

11β-羟基类固醇脱氢酶 1 型 (11β-HSD1) 可相互转化无活性的糖皮质激素可的松及其活性形式的皮质醇。它被广泛表达，虽然是双向的，但在体内它主要作为一种氧化还原酶发挥作用，产生活性糖皮质激素。这允许以组织特异性方式在前受体水平调节糖皮质激素受体激活。在这篇综述中，我们将讨论 11β-HSD1 的酶学和分子生物学以及可的松还原酶缺陷的分子基础。我们还将讨论 11β-HSD1 活性的改变如何与许多疾病状态有关，我们将探讨其在不同组织的生理学和病理学中的作用。最后，我们将讨论选择性 11β-HSD1 抑制剂的现状，这些抑制剂正在开发中，并在代谢综合征患者的 II 期试验中进行测试。尽管数据是初步的，但 11β-HSD1 的治疗性抑制对于治疗各种其他疾病（如骨质疏松症、青光眼、颅内高压和认知能力下降）也是一个令人兴奋的前景。