11β-HSD2

更新于：2025-05-07

基本信息

别名

11-beta-HSD type II、11-beta-HSD2、11-beta-hydroxysteroid dehydrogenase type 2

+ [10]

简介

Catalyzes the conversion of biologically active 11beta-hydroxyglucocorticoids (11beta-hydroxysteroid) such as cortisol, to inactive 11-ketoglucocorticoids (11-oxosteroid) such as cortisone, in the presence of NAD(+) (PubMed:10497248, PubMed:12788846, PubMed:17314322, PubMed:22796344, PubMed:27927697, PubMed:30902677, PubMed:33387577, PubMed:7859916, PubMed:8538347). Functions as a dehydrogenase (oxidase), thereby decreasing the concentration of active glucocorticoids, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids (PubMed:10497248, PubMed:12788846, PubMed:17314322, PubMed:33387577, PubMed:7859916). Plays an important role in maintaining glucocorticoids balance during preimplantation and protects the fetus from excessive maternal corticosterone exposure (By similarity). Catalyzes the oxidation of 11beta-hydroxytestosterone (11beta,17beta-dihydroxyandrost-4-ene-3-one) to 11-ketotestosterone (17beta-hydroxyandrost-4-ene-3,11-dione), a major bioactive androgen (PubMed:22796344, PubMed:27927697). Catalyzes the conversion of 11beta-hydroxyandrostenedione (11beta-hydroxyandrost-4-ene-3,17-dione) to 11-ketoandrostenedione (androst-4-ene-3,11,17-trione), which can be further metabolized to 11-ketotestosterone (PubMed:27927697). Converts 7-beta-25-dihydroxycholesterol to 7-oxo-25-hydroxycholesterol in vitro (PubMed:30902677). 7-beta-25-dihydroxycholesterol (not 7-oxo-25-hydroxycholesterol) acts as a ligand for the G-protein-coupled receptor (GPCR) Epstein-Barr virus-induced gene 2 (EBI2) and may thereby regulate immune cell migration (PubMed:30902677). May protect ovulating oocytes and fertilizing spermatozoa from the adverse effects of cortisol (By similarity).

关联

100 项与 11β-HSD2 相关的临床结果

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100 项与 11β-HSD2 相关的转化医学

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0 项与 11β-HSD2 相关的专利（医药）

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1,461

项与 11β-HSD2 相关的文献（医药）

2025-12-31·Epigenetics

A polyepigenetic glucocorticoid exposure score and HPA axis-related DNA methylation are associated with gestational epigenetic aging

Article

作者: Appleton, Allison A.

Gestational epigenetic aging (GEA) is a novel approach for characterizing associations between prenatal exposures and postnatal risks. Psychosocial adversity in pregnancy may influence GEA, but the molecular mechanisms are not well understood. DNA methylation to glucocorticoid regulation and hypothalamic-pituitary-adrenal (HPA) axis genes are implicated but have not been fully examined in association with GEA. This study investigated whether a polyepigenetic glucocorticoid exposure score (PGES) and HPA axis gene (NR3C1, HSD11B2, FKBP5) methylation were associated with GEA, and whether associations were sex-specific. Participants were from a prospective cohort of racial/ethnic diverse and socially disadvantaged pregnant women and infants (n = 200). DNA methylation variables were estimated using umbilical cord blood. PGES was derived with CpGs shown to be sensitive to synthetic dexamethasone exposure. NR3C1, HSD11B2, and FKBP5 methylation was summarized via factor analysis. We found that PGES (β = -1.12, SE = 0.47, p = 0.02) and several NR3C1 and FKBP5 factor scores were associated with decelerated GEA (all p < 0.05). A significant sex interaction was observed for FKBP5 factor score 3 (β = -0.34, SE = 0.15, p = 0.02) suggesting decelerated GEA for males but not females. This study showed that glucocorticoid regulation-related DNA methylation was associated with a decelerated aging phenotype at birth that might indicate a neonatal risk.

2025-07-01·The Journal of Steroid Biochemistry and Molecular Biology

Production of 11-ketotestosterone in childhood adrenal tumors with virilization or peripheral precocious puberty: Dominant expression of 11β-hydroxysteroid dehydrogenase type 2

Article

作者: Fujisawa, Yasuko ; Sakaguchi, Kimiyoshi ; Murai, Yuki ; Kinjo, Kenichi ; Oyama, Ibuki ; Ogata, Tsutomu ; Ikeda, Maiko ; Tanikawa, Wataru ; Masunaga, Yohei ; Sano, Shinichiro

11-Oxygenated androgens are important components of the androgen pool in humans. Among them, 11-ketotestosterone (11-KT), a potent 11-oxygenated androgen primarily produced in peripheral tissues outside the adrenal glands, has garnered research interest for its crucial role in several diseases associated with androgen excess. This study aimed to investigate the biosynthesis of 11-oxygenated androgens, particularly 11-KT, in childhood adrenocortical tumors (ACTs) presenting with symptoms of androgen excess. This retrospective study included three patients, aged 6 months, 2 years, and 12 years, presenting with symptoms of androgen excess due to childhood ACTs. Multiple androgen metabolites were simultaneously measured using pre- or postoperative serum samples, tumors, and tumor-attached adrenal glands obtained from patients using liquid chromatography-tandem mass spectrometry. The expression of genes involved in androgen synthesis was analyzed using DNA microarray analysis. Serum androgen levels were elevated prior to tumor removal and decreased to within or near reference ranges after tumor removal. Notably, serum 11-KT levels were markedly elevated compared to reference ranges, similar to testosterone (T), and 11-KT was abundant within the tumor tissues. Unique gene expression patterns were observed across the three cases of childhood ACTs, including marked HSD11B2, attenuated HSD11B1, and elevated HSD17B3 expression levels, which are involved in 11-KT biosynthesis. This study confirms the direct production of 11-KT in childhood ACTs; gene expression patterns observed in these cases favored 11-KT biosynthesis, providing insight into their potential role in androgen excess.

2025-05-01·Clinical Nephrology

Unraveling hypertension through mineralocorticoid receptor activation in Cushing’s syndrome: A case report

Article

作者: Hommos, Musab S. ; Westphal, Sydney ; Thomson, Holly

BACKGROUNDCushing's syndrome is a rare cause of secondary hypertension. There are several mechanisms reported as contributing factors for blood pressure elevation in hypercortisolism patients. This case highlights the central role of mineralocorticoid receptors' activation by the excess cortisol in the development of hypertension.CASE PRESENTATIONA 45-year-old male presented with several months of cushingoid features and refractory hypertension on maximum doses of five antihypertensive drugs, not including a mineralocorticoid receptor blocker. Workup for other causes of secondary hypertension revealed sleep apnea but was otherwise negative. Further evaluation revealed a carcinoid lung tumor as the cause of Cushing's syndrome with its ectopic production of adrenocorticotropic hormone (ACTH). Prior to the resection of this tumor, the addition of eplerenone, a mineralocorticoid receptor blocker, resulted in significant improvement in blood pressure within 4 weeks, highlighting that cortisol activation of mineralocorticoid receptors is one of the main mechanisms of hypertension in this patient with hypercortisolism.CONCLUSIONIn hypercortisolism patients, some excess cortisol escapes deactivation by the 11β-hydroxysteroid dehydrogenase 2 enzyme in the kidney and directly activates mineralocorticoid receptors. Recent literature suggests that specific patient populations have subtle elevations in cortisol levels, and cortisol's effect on end-organ damage follows a spectrum from high-normal cortisol to overt hypercortisolism. Other data suggest a decline in 11β-hydroxysteroid dehydrogenase 2 enzyme activity with age. Additional research is needed to further define the role of cortisol-mineralocorticoid receptor interaction in hypertension among patients without overt hypercortisolism but with high-normal cortisol or low 11β-hydroxysteroid dehydrogenase 2 enzymatic activity.

项与 11β-HSD2 相关的新闻（医药）

2023-12-08

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