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Is AMH a regulator of follicular atresia?

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Abstract

We discuss the hypothesis that AMH is an intraovarian regulator that inhibits follicular atresia within the human ovary. Several indirect lines of evidence derived from clinical and basic science studies in a variety of different patient populations and model systems collectively support this hypothesis. Evidence presented herein include 1) timing of onset of menopause in women with polycystic ovary syndrome, 2) site of cellular origin and timing of AMH production, 3) AMH’s influence on other critical growth factors and enzymes involved in folliculogenesis, and 4) AMH’s inhibition of granulosa apoptosis. If this hypothesis is true, it may provide insight for treatment strategies for prevention and treatment of premature ovarian insufficiency, slowing natural ovarian aging, and/or delaying eventual ovarian failure. Such findings may lead to the development of 1) AMH agonists for retarding the onset of menopause and/or as a chemoprotectant prior to cancer therapy and 2) AMH antagonists for the treatment of PCOS.

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Grants

American Society for Reproductive Medicine and Ferring Pharamceuticals to Z.M.

Disclosure

D.B.S. received royalties from a licensing agreement between Rutgers Medical School/MGH and Beckman Coulter for the use of AMH in determining ovarian reserve.

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Correspondence to Zaher Merhi.

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Evidence suggests that AMH may represent a significant regulator of follicular atresia in the human ovary.

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Seifer, D.B., Merhi, Z. Is AMH a regulator of follicular atresia?. J Assist Reprod Genet 31, 1403–1407 (2014). https://doi.org/10.1007/s10815-014-0328-7

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  • DOI: https://doi.org/10.1007/s10815-014-0328-7

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