{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n HSD11B2 encodes the enzyme 11β‐hydroxysteroid dehydrogenase type 2, which catalyzes the conversion of active glucocorticoids (cortisol in humans) into their inactive forms (cortisone). This conversion is essential for protecting the mineralocorticoid receptor from inadvertent activation by glucocorticoids and thereby conferring specificity for aldosterone in tissues such as the kidney and colon."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In the placenta, HSD11B2 is expressed in the trophoblast layer where it functions as a critical “barrier” that limits fetal exposure to elevated maternal glucocorticoids. Reduced placental expression or activity—whether through maternal stress, adverse socioeconomic conditions, environmental toxicants like cadmium, hypoxia, or epigenetic modifications—has been linked with altered fetal growth, impaired neurodevelopment, and long‐term programming of blood pressure and metabolic regulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "5", "end_ref": "14"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Genetic and epigenetic variation in HSD11B2 has further been implicated in the regulation of salt sensitivity and blood pressure. Specific promoter polymorphisms and single‐nucleotide variations have been associated with reduced enzyme activity and a higher cortisol/cortisone ratio, mechanisms that contribute to conditions such as apparent mineralocorticoid excess and salt‐sensitive hypertension."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "15", "end_ref": "18"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In addition, HSD11B2 expression in the developing brain is pivotal for neuroprotection; by inactivating glucocorticoids, it safeguards neural progenitors from the potentially deleterious effects of excessive glucocorticoid exposure, thus contributing to normal cerebellar and central nervous system development."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "19"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Moreover, in nonrenal tissues such as the cardiovascular system, altered HSD11B2 activity contributes to adverse remodelling, inflammation, and ultimately atherosclerotic and fibrotic changes. Collectively, these multifaceted roles underscore HSD11B2’s function as a critical prereceptor regulator of glucocorticoid action, ensuring proper mineralocorticoid receptor activation, maintenance of electrolyte balance, and normal fetal programming. Alterations in its expression or activity—whether due to environmental influences, maternal stress, or genetic polymorphisms—can have profound consequences for postnatal cardiovascular, renal, and neurobehavioral health."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "24"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Overall, HSD11B2 is indispensable for glucocorticoid metabolism and represents a key molecular node linking the intrauterine environment to long‐term health outcomes, including blood pressure regulation, neurodevelopment, and cardiovascular homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "35"}]}, {"type": "t", "text": "\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Rasoul Alikhani-Koopaei, Fatemeh Fouladkou, Felix J Frey, et al. 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