{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T14:04:47Z","timestamp":1790172287139,"version":"4.1.0"},"reference-count":95,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T00:00:00Z","timestamp":1790121600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Endocrinol."],"abstract":"<jats:p>\n                    PCOS, the leading cause of female infertility, affects 4 to 21% of women in age to give birth. Despite numerous investigations aimed at understanding the syndrome, its origin(s) remains unknown. This paper reports neglected or overlooked studies and seeks to integrate them within the relevant literature. Data presented herein strongly suggests that a modified Pro-\u03b1C inhibin (featuring a deletion of the 15 N-terminal amino acids of \u03b1C domain: \u201cPro-\u25b51-15-\u03b1C inhibin\u201d) suppresses GnRH pulses (\u201cGnRH-Statin activity\u201d)\n                    <jats:italic>in vivo<\/jats:italic>\n                    and GnRH secretion\n                    <jats:italic>in vitro<\/jats:italic>\n                    . Pro-\u03b1C inhibin, an \u03b1 inhibin gene product devoid of \u03b2A\/\u03b2B inhibin domains and lacking inhibin or activin activity is present in follicular fluid and serum and is strongly expressed in luteal cells. A SNP, changing cysteine at position 1 to serine in the \u03b1 inhibin gene Pro-domain was identified in a human polycystic ovary, in contrast to human placenta and a human macrophage cell line. This mutation which disrupts the S-S bridge linking the Pro and \u03b1C inhibin domains of Pro-\u25b51-15-\u03b1C inhibin or Pro-\u03b1C inhibin, is hypothesized to induce a loss-of-function. The hypothesis proposed is the following: such a loss-of-function could induce an over-activity of GnRH neurons, that has been shown to induce PCOS-like reproductive traits in female mice. Overall, if experimentally verified, this hypothesis could constitute a breakthrough in understanding the long sought after etiology (or ethiologies) for a subset of reproductive PCOS phenotypes. Furthermore, beyond the SNP hypothesis, the paper revisits Pro-\u03b1C inhibin-related molecules and their activities.\n                  <\/jats:p>","DOI":"10.3389\/fendo.2026.1909939","type":"journal-article","created":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T13:23:57Z","timestamp":1790169837000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["A challenging hypothesis: can a SNP changing cysteine 1 in the \u03b1 inhibin pro-domain induce reproduction-linked PCOS phenotypes?"],"prefix":"10.3389","volume":"17","author":[{"given":"Michel Roger","family":"Blanc","sequence":"first","affiliation":[{"name":"Laboratoire de Neuroendocrinologie Sexuelle, Institut National de la Recherche pour l'Agriculture, l'Alimentation et l'Environnement (INRA) Centre Val de Loire","place":["Nouzilly, 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