Control hormonal y molecular del desarrollo de la glándula prostática
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El control del crecimiento y de la fisiología prostática está basado en complejas interacciones de hormonas esteroides; específicamente son las vías metabólicas de su biosíntesis y degradación las que intervienen en el desarrollo de la glándula. También participan hormonas peptídicas y factores de crecimiento e interacciones entre el epitelio y el estroma. El desarrollo de la glándula prostática es caracterizado por una etapa de inducción prenatal, de ramificación ductal, diferenciación celular posnatal y otra de crecimiento durante la pubertad, esta última consecuencia de la producción testicular de testosterona (T). La conversión de T en dihidrotestosterona (DHT), por la acción de la enzima 5-α-reductasa, es importante en el origen embrionario de la glándula. Esta dependencia androgénica es también demostrada en el adulto, donde la privación de esta hormona lleva a una drástica regresión de la glándula. Además de andrógenos, otras hormonas como la progesterona y los estrógenos poseen acciones importantes en la fisiología prostática. Particularmente, este último es un factor regulador durante el desarrollo normal de la glándula, pero en determinadas situaciones se le ha asociado como agente inductor de algunas patologías durante el envejecimiento. Finalmente, la acción de enzimas como la aromatasa y de otras relacionadas con la conversión de T y de la DHT en compuestos sin actividad androgenica, como la 3β-hidroxi-esteroide deshidrogenasa (3β-HSD) y la 3β-adiol-hidroxilasa (CYP7B1) junto con la expresión coordinada de los receptores de hormonas esteroides ofrecen el equilibrio necesario para el desarrollo prostático normal. Esta revisión se centra en la acción de hormonas esteroides en diferentes etapas del desarrollo prostático, y aborda la acción de disruptores endocrinos.
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