P66 | FROM INNERVATION TO STEROIDOGENIC DEFECT: IMPLICATIONS OF CGRP IN THE PATHOPHYSIOLOGY OF POLYCYSTIC OVARY SYNDROME

Polycystic ovary syndrome (PCOS) is a multifactorial endocrine disorder affecting up to 20% of women of reproductive age. It is characterized by hyperandrogenism, menstrual irregularities, anovulation, and metabolic disturbances, including insulin resistance and increased cardiometabolic risk1. Alt...

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Published: PAGEPress Publications 2025-08-01
Series:European Journal of Histochemistry
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Online Access:https://www.ejh.it/ejh/article/view/4391
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description Polycystic ovary syndrome (PCOS) is a multifactorial endocrine disorder affecting up to 20% of women of reproductive age. It is characterized by hyperandrogenism, menstrual irregularities, anovulation, and metabolic disturbances, including insulin resistance and increased cardiometabolic risk1. Although its pathogenesis remains unclear, recent studies suggest a potential role for neuropeptides in modulating ovarian function2. This study aims to investigate the presence of calcitonin gene related peptide (CGRP), a 37-amino-acid neuropeptide involved in vasodilation, nociceptive signaling, and modulation of the inflammatory response3, within the ovary and follicular fluid of women with PCOS. CGRP levels were quantified in follicular fluid from PCOS (n=27) and non-PCOS (n=27) women, showing significantly higher concentrations in the PCOS group (p<0.05). Immunohistochemistry analyses revealed intense CGRP immunoreactivity surrounding preantral follicles in PCOS ovaries, particularly around the theca cell layer. In contrast, non-PCOS samples exhibited weaker CGRP expression. This differential pattern suggests a possible involvement of CGRP in early follicular development. The altered follicular microenvironment in PCOS may permit the accumulation of small neuropeptides like CGRP, which could exert autocrine/paracrine effects on follicular cells, influencing both development and steroidogenesis4. To further investigate this hypothesis, we assessed the effects of CGRP on cell viability, mitochondrial and steroidogenic activity in primary h-GCs. These findings suggest that CGRP may contribute to the dysregulation of follicular development observed in PCOS. A better understanding of its role could offer new insights for the development of targeted therapies aimed at restoring ovarian function in affected women.
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series European Journal of Histochemistry
spelling doaj-art-e4a208c9db1d42a28b4be4aa9ddcd3a42025-08-23T11:18:35ZengPAGEPress PublicationsEuropean Journal of Histochemistry1121-760X2038-83062025-08-0169s210.4081/ejh.2025.4391P66 | FROM INNERVATION TO STEROIDOGENIC DEFECT: IMPLICATIONS OF CGRP IN THE PATHOPHYSIOLOGY OF POLYCYSTIC OVARY SYNDROME Polycystic ovary syndrome (PCOS) is a multifactorial endocrine disorder affecting up to 20% of women of reproductive age. It is characterized by hyperandrogenism, menstrual irregularities, anovulation, and metabolic disturbances, including insulin resistance and increased cardiometabolic risk1. Although its pathogenesis remains unclear, recent studies suggest a potential role for neuropeptides in modulating ovarian function2. This study aims to investigate the presence of calcitonin gene related peptide (CGRP), a 37-amino-acid neuropeptide involved in vasodilation, nociceptive signaling, and modulation of the inflammatory response3, within the ovary and follicular fluid of women with PCOS. CGRP levels were quantified in follicular fluid from PCOS (n=27) and non-PCOS (n=27) women, showing significantly higher concentrations in the PCOS group (p<0.05). Immunohistochemistry analyses revealed intense CGRP immunoreactivity surrounding preantral follicles in PCOS ovaries, particularly around the theca cell layer. In contrast, non-PCOS samples exhibited weaker CGRP expression. This differential pattern suggests a possible involvement of CGRP in early follicular development. The altered follicular microenvironment in PCOS may permit the accumulation of small neuropeptides like CGRP, which could exert autocrine/paracrine effects on follicular cells, influencing both development and steroidogenesis4. To further investigate this hypothesis, we assessed the effects of CGRP on cell viability, mitochondrial and steroidogenic activity in primary h-GCs. These findings suggest that CGRP may contribute to the dysregulation of follicular development observed in PCOS. A better understanding of its role could offer new insights for the development of targeted therapies aimed at restoring ovarian function in affected women. https://www.ejh.it/ejh/article/view/4391-
spellingShingle P66 | FROM INNERVATION TO STEROIDOGENIC DEFECT: IMPLICATIONS OF CGRP IN THE PATHOPHYSIOLOGY OF POLYCYSTIC OVARY SYNDROME
European Journal of Histochemistry
-
title P66 | FROM INNERVATION TO STEROIDOGENIC DEFECT: IMPLICATIONS OF CGRP IN THE PATHOPHYSIOLOGY OF POLYCYSTIC OVARY SYNDROME
title_full P66 | FROM INNERVATION TO STEROIDOGENIC DEFECT: IMPLICATIONS OF CGRP IN THE PATHOPHYSIOLOGY OF POLYCYSTIC OVARY SYNDROME
title_fullStr P66 | FROM INNERVATION TO STEROIDOGENIC DEFECT: IMPLICATIONS OF CGRP IN THE PATHOPHYSIOLOGY OF POLYCYSTIC OVARY SYNDROME
title_full_unstemmed P66 | FROM INNERVATION TO STEROIDOGENIC DEFECT: IMPLICATIONS OF CGRP IN THE PATHOPHYSIOLOGY OF POLYCYSTIC OVARY SYNDROME
title_short P66 | FROM INNERVATION TO STEROIDOGENIC DEFECT: IMPLICATIONS OF CGRP IN THE PATHOPHYSIOLOGY OF POLYCYSTIC OVARY SYNDROME
title_sort p66 from innervation to steroidogenic defect implications of cgrp in the pathophysiology of polycystic ovary syndrome
topic -
url https://www.ejh.it/ejh/article/view/4391