Endometrial hyperplasia is most directly associated with signaling through which receptor?

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Multiple Choice

Endometrial hyperplasia is most directly associated with signaling through which receptor?

Explanation:
Endometrial hyperplasia results from estrogen signaling through the estrogen receptor, which acts as a nuclear transcription factor to drive endometrial cell proliferation. When estrogen binds its receptor in the endometrium, it promotes transcription of genes that push the glands and stroma to grow, increasing glandular density and thickening of the lining. In a normal cycle, progesterone dampens this proliferative effect and promotes secretory maturation, helping to limit unchecked growth. When estrogen is unopposed—such as with anovulatory cycles, obesity with more peripheral estrogen production, or estrogen therapy without progestin—the proliferative signal via the estrogen receptor runs unchecked, leading to endometrial hyperplasia. The other receptors listed are not the primary drivers of this proliferative change in the endometrium.

Endometrial hyperplasia results from estrogen signaling through the estrogen receptor, which acts as a nuclear transcription factor to drive endometrial cell proliferation. When estrogen binds its receptor in the endometrium, it promotes transcription of genes that push the glands and stroma to grow, increasing glandular density and thickening of the lining. In a normal cycle, progesterone dampens this proliferative effect and promotes secretory maturation, helping to limit unchecked growth. When estrogen is unopposed—such as with anovulatory cycles, obesity with more peripheral estrogen production, or estrogen therapy without progestin—the proliferative signal via the estrogen receptor runs unchecked, leading to endometrial hyperplasia. The other receptors listed are not the primary drivers of this proliferative change in the endometrium.

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