Implications and Future Perspectives of AGEs in PCOS Pathophysiology

Επιστημονική δημοσίευση - Άρθρο Περιοδικού uoadl:3077601 10 Αναγνώσεις

Μονάδα:
Ερευνητικό υλικό ΕΚΠΑ
Τίτλος:
Implications and Future Perspectives of AGEs in PCOS Pathophysiology
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Human, animal, and in vitro studies provide evidence that advanced glycation end-products (AGEs) may contribute to the pathogenesis of polycystic ovary syndrome (PCOS) and its metabolic and reproductive consequences. AGEs are able to induce, via activation of key intracellular signaling pathways, the generation of oxidative stress and proinflammatory cytokines, thus contributing to the adverse health impact of PCOS. This review presents the implications of AGEs in several disease pathophysiologies, including PCOS, as well as the cellular and systemic effects of AGEs on insulin resistance (IR), hyperandrogenemia, endoplasmic reticulum (ER) stress, hypoxia, and ovarian function. The gaps in our knowledge will serve as launching pad for future developments ranging from dietary and lifestyle changes to pharmaceutical interventions aiming at potential applications in women with PCOS. © 2019 Elsevier Ltd
Έτος δημοσίευσης:
2019
Συγγραφείς:
Merhi, Z.
Kandaraki, E.A.
Diamanti-Kandarakis, E.
Περιοδικό:
TRENDS IN ENDOCRINOLOGY AND METABOLISM
Εκδότης:
W B SAUNDERS CO-ELSEVIER INC
Τόμος:
30
Αριθμός / τεύχος:
3
Σελίδες:
150-162
Λέξεις-κλειδιά:
advanced glycation end product; advanced glycation end product receptor; advanced glycation end product; advanced glycation end product receptor, endoplasmic reticulum stress; human; hyperandrogenism; hypoxia; insulin resistance; ovary function; ovary polycystic disease; pathophysiology; priority journal; Review; signal transduction; animal; female; metabolism; ovary polycystic disease; pathophysiology; physiology, Animals; Female; Glycation End Products, Advanced; Humans; Insulin Resistance; Polycystic Ovary Syndrome; Receptor for Advanced Glycation End Products
Επίσημο URL (Εκδότης):
DOI:
10.1016/j.tem.2019.01.005
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