2015
DOI: 10.1007/s12020-015-0715-6
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Role of the steroidogenic acute regulatory protein in health and disease

Abstract: Steroid hormones are an important class of regulatory molecules that are synthesized in steroidogenic cells of the adrenal, ovary, testis, placenta, brain and skin, and influence a spectrum of developmental and physiological processes. The steroidogenic acute regulatory protein (STAR) predominantly mediates the rate-limiting step in steroid biosynthesis, i.e., the transport of the substrate of all steroid hormones, cholesterol, from the outer to the inner mitochondrial membrane. At the inner membrane, cytochro… Show more

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Cited by 156 publications
(114 citation statements)
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References 223 publications
(295 reference statements)
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“…D, the follicular development‐related genes Gdf9 , Bmp15 , and Amhr2 did not change, while genes related to steroid hormone synthesis, especially Star and Lhr, declined dramatically in Rapa‐treated ovaries. As these two genes play crucial roles in P4 synthesis, and LHR (the receptor for LH and HCG [human chorionic gonadotropin]) is also indispensable for ovulation (Ascoli et al ., ; Manna et al ., ), such declines can be explained by the decrease in serum P4 levels and anovulation after Rapa treatment. Interleukins or sirtuins that are involved in the process of aging (Minciullo et al ., ; Grabowska et al ., ) were also evaluated, and IL‐1 α, IL‐6, and Sirt3 showed dramatic changes after Rapa administration.…”
Section: Resultsmentioning
confidence: 96%
“…D, the follicular development‐related genes Gdf9 , Bmp15 , and Amhr2 did not change, while genes related to steroid hormone synthesis, especially Star and Lhr, declined dramatically in Rapa‐treated ovaries. As these two genes play crucial roles in P4 synthesis, and LHR (the receptor for LH and HCG [human chorionic gonadotropin]) is also indispensable for ovulation (Ascoli et al ., ; Manna et al ., ), such declines can be explained by the decrease in serum P4 levels and anovulation after Rapa treatment. Interleukins or sirtuins that are involved in the process of aging (Minciullo et al ., ; Grabowska et al ., ) were also evaluated, and IL‐1 α, IL‐6, and Sirt3 showed dramatic changes after Rapa administration.…”
Section: Resultsmentioning
confidence: 96%
“…Mitochondrial damage is associated with dysfunction of LCs, which are involved mainly in the production and secretion of testosterone. 32,33 Dysfunction of primary cultured rat LCs induced by nano-TiO 2 may be triggered via downregulation of ERK-pathway-related factor proteins, such as pERK1/2, PKA, and PKC ( Figures 11C-H and 12C), steroidogenic factor proteins, such as StAR, 3βHSD, P450scc, and SR-BI, and concomitant upregulation of DAX1 ( Figure 13).…”
Section: Discussionmentioning
confidence: 99%
“…30 StAR modulates the transfer of cholesterol from the cytoplasm to mitochondria, regarded as the rate-limiting step in steroidhormone synthesis. [31][32][33][34][35][36] Limited studies to date have focused on the molecular mechanisms underlying the effects of nano-TiO 2 on testosterone generation.…”
Section: Introductionmentioning
confidence: 99%
“…) (Miller and Auchus ; Turcu and Auchus ; Manna et al. ). Acquired causes, include infectious diseases (Waterhouse‐Frederichsen syndrome), vascular diseases (hemorrhage and coagulopathy), surgery (bilateral adrenalectomy), and exposure to certain medications (rifampicin, phenytoin, and ketoconazole) (Zaloga and Marik ).…”
Section: Discussionmentioning
confidence: 99%
“…Congenital causes include autosomal recessive congenital lipoid adrenal hyperplasia (CAH, MIM# 201710) (caused by pathogenic variants in STAR); congenital adrenal insufficiency with partial or complete 46XY sex reversal (AICSR, MIM# 613743) (caused by variants in CYP11A1), congenital adrenal hyperplasia due to 3b-hydroxysteroid dehydrogenase 2 deficiency (caused by variants in HSD3B2); congenital adrenal hyperplasia due to 21-hydroxylase deficiency (MIM# 201910) (caused by variants in CYP21A2); 11b-hydroxylase deficiency (caused by variants in CYP11B1) which can result in autosomal recessive congenital adrenal hyperplasia (MIM# 202010) or autosomal dominant glucocorticoidremediable aldosteronism (MIM# 103900); 17-a-hydroxylase/17,20-lyase deficiency (MIM# 202110) (caused by variants in CYP17A1); P450 oxidoreductase deficiency (MIM# 201750) (caused by variants in POR) (Katsumata et al 2002;Hiort et al 2005;Slominski et al 2015); familial glucocorticoid deficiency (FGD) (caused by defects in STAR, MC2R, MRAP, MCM4, NNT, TXNRD2, GPX1 and PRDX3) (Miller 2017); and autoimmune disorders such as polyendocrinopathy syndrome type I, with or without reversible metaphyseal dysplasia (MIM# 240300, caused by defects in AIRE) (Fig. 2) (Miller and Auchus 2011;Turcu and Auchus 2015;Manna et al 2016). Acquired causes, include infectious diseases (Waterhouse-Frederichsen syndrome), vascular diseases (hemorrhage and coagulopathy), surgery (bilateral adrenalectomy), and exposure to certain medications (rifampicin, phenytoin, and ketoconazole) (Zaloga and Marik 2001).…”
Section: Discussionmentioning
confidence: 99%