{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSteroid sulfatase (STS) is a pivotal enzyme in steroid hormone metabolism that acts by cleaving sulfate groups from a wide array of steroid sulfates, thereby converting these inactive conjugates into biologically active steroids. This desulfation process is essential for maintaining the dynamic balance of hormone action in the endocrine system, and its activity can influence systemic as well as local steroid concentrations, impacting multiple physiologic processes such as sexual development, energy homeostasis, and reproductive function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nStructural and cellular studies have revealed that STS is a membrane‐bound enzyme with a unique “mushroom‐like” architecture that positions its active site near the lipid bilayer. In specialized tissues such as the placenta and hair follicles, the enzyme is strategically localized to modulate local steroid production—for instance, facilitating the conversion of estrone sulfate to estrone in the placenta and contributing to the intrafollicular formation of active androgens. These local actions underscore its critical role in regulating tissue‐specific hormone concentrations."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "4", "end_ref": "7"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAlterations in STS function—whether by genetic mutations or dysregulated expression—have significant pathological consequences. Loss‐of-function mutations in the STS gene on the X chromosome, for example, cause X‐linked ichthyosis, a condition characterized by the accumulation of cholesterol sulfate in the epidermis and associated scaling and barrier abnormalities. Moreover, aberrant STS activity has been implicated in a spectrum of estrogen‐dependent diseases such as endometriosis, various hormone‐responsive cancers (breast, endometrial, ovarian, and prostate), and even neurodevelopmental disorders including attention deficit hyperactivity disorder. In polycystic ovarian syndrome (PCOS), changes in the expression of STS appear to contribute to local estrogen imbalances. Collectively, these findings point to an intricate association between STS and disease, where both increased and decreased enzyme activity can disrupt normal steroid signaling."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "8", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its direct catalytic role, STS is subject to complex regulation by numerous factors in different tissues. In the brain, strong STS expression within cortical neurons facilitates the conversion of circulating neurosteroid sulfates such as dehydroepiandrosterone sulfate (DHEAS) into active neurosteroids, a process that may influence neurodevelopment and cognitive function. Inflammatory cytokines (e.g., interleukin‐1β) and growth factors (e.g., IGF‐II) have been shown to modulate STS expression via intracellular signaling pathways (including PI3-kinase/Akt and NF-κB), while genetic variations in STS also modify its expression and activity in a tissue-specific manner. These regulatory mechanisms likely enable STS to respond to diverse physiologic cues, thereby fine-tuning local steroid bioavailability in tissues such as the vascular smooth muscle, adipose tissue, and various brain regions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "29", "end_ref": "38"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, STS can influence broader aspects of steroidogenesis. For example, studies have demonstrated that increased STS activity can enhance the translation and stabilization of key proteins such as the steroidogenic acute regulatory (StAR) protein, thereby amplifying the production of steroids from cholesterol substrates. Such cross‐talk underscores the enzyme’s central role in coordinating the supply of active steroids with cellular energy and metabolic demands, and it highlights why both pharmacological inhibitors of STS and genetic variations in its expression are being actively investigated as therapeutic targets."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "39"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jonathan W Mueller, Lorna C Gilligan, Jan Idkowiak, et al. 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