The DOI matches its Crossref record; 359 of the 359 references it cites were found in a registry or an index.
Animal Models to Understand the Etiology and Pathophysiology of Polycystic Ovary Syndrome
Open accessAbstract
More than 1 out of 10 women worldwide are diagnosed with polycystic ovary syndrome (PCOS), the leading cause of female reproductive and metabolic dysfunction. Despite its high prevalence, PCOS and its accompanying morbidities are likely underdiagnosed, averaging > 2 years and 3 physicians before women are diagnosed. Although it has been intensively researched, the underlying cause(s) of PCOS have yet to be defined. In order to understand PCOS pathophysiology, its developmental origins, and how to predict and prevent PCOS onset, there is an urgent need for safe and effective markers and treatments. In this review, we detail which animal models are more suitable for contributing to our understanding of the etiology and pathophysiology of PCOS. We summarize and highlight advantages and limitations of hormonal or genetic manipulation of animal models, as well as of naturally occurring PCOS-like females.
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Cites
Finding the missing heritability of complex diseases
Manolio, T. A., Collins, F. S., Cox, N. J., Goldstein, D. B., Hindorff, L. A., Hunter, D. J., McCarthy, M. I., Ramos, E. M., Cardon, L. R., Chakravarti, A., et al. (2009) · Nature · doi:10.1038/nature08494 · Cited by 8,336 · cited 1×
“One possible explanation is that common genetic variants detected by GWAS have small biological effects, whereas rare genetic variants identified with whole-genome sequencing (WGS) or whole-exome sequencing (WES), likely have larger biological effects in complex diseases such as PCOS (203).”
BackgroundThe Diagnosis of Polycystic Ovary Syndrome during Adolescence
Witchel, S. F., Oberfield, S., Rosenfield, R. L., Codner, E., Bonny, A., Ibáñez, L., Pena, A., Horikawa, R., Gomez-Lobo, V., Joel, D., et al. (2015) · Hormone Research in Paediatrics · doi:10.1159/000375530 · Cited by 3,113
The origins of the developmental origins theory
Barker, D. J. P. (2007) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2007.01809.x · Cited by 2,955
Polycystic Ovary Syndrome: Definition, Aetiology, Diagnosis and Treatment
Escobar-Morreale, H. F. (2018) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2018.24 · Cited by 2,083
Diamanti-Kandarakis, E., & Dunaif, A. (2012) · Endocrine Reviews · doi:10.1210/er.2011-1034 · Cited by 1,947
Lubahn, D. B., Moyer, J. S., Golding, T. S., Couse, J. F., Korach, K. S., & Smithies, O. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.23.11162 · Cited by 1,898
Teede, H. J., Misso, M. L., Costello, M. F., Dokras, A., Laven, J., Moran, L., Piltonen, T., Norman, R. J., & the International PCOS Network (2018) · Clinical Endocrinology · doi:10.1111/cen.13795 · Cited by 1,823
Rosenfield, R. L., & Ehrmann, D. A. (2016) · Endocrine Reviews · doi:10.1210/er.2015-1104 · Cited by 1,603
Teede, H. J., Misso, M. L., Costello, M. F., Dokras, A., Laven, J., Moran, L., Piltonen, T., Norman, R. J., International PCOS Network, Andersen, M., et al. (2018) · Human Reproduction · doi:10.1093/humrep/dey256 · Cited by 1,593
Self-citationBozdag, G., Mumusoglu, S., Zengin, D., Karabulut, E., & Yildiz, B. O. (2016) · Human Reproduction · doi:10.1093/humrep/dew218 · Cited by 1,526
Research works printed but not linked: 13
- Mahesh, 1982, The polycystic ovary syndrome and experimental models for the study of its pathogenesis, Prog Clin Biol Res., 112 Pt A, 301
- 17, 2020, Animal models to understand the etiology and pathophysiology of polycystic ovary syndrome, Dryad
- Abbott, 2006, Animal models and fetal programming of the polycystic ovary syndrome, 259
- Goy, 1982, Prenatal exposure of rhesus monkeys to patent androgens: morphological, behavioral, and physiological conse- quences, 355
- Lee, 2003, Fetal programming: prenatal exposure to testosterone disrupts FSH dynamics during the sheep estrous cycle, Biol Reprod., 68, 366
- Matzuk, 2003, Overexpression of human chorionic gonadotropin causes multiple reproductive defects in transgenic mice, Biol Reprod., 69, 338, 10.1095/biolreprod.102.013953 · doi:10.1095/biolreprod.102.013953
- Riepsamen, 2019, Serum concentrations of oocyte-secreted factors BMP15 and GDF9 during IVF and in women with reproductive pathologies, Endocrinology., 160, 2298, 10.1210/en.2019-00264 · doi:10.1210/en.2019-00264
- Russell, 2016, Bidirectional communication between cumulus cells and the oocyte: old hands and new players?, Theriogenology., 86, 62, 10.1016/j.theriogenology.2016.04.019 · doi:10.1016/j.theriogenology.2016.04.019
- Peluso, 2015, AMH and AMHR2 polymorphisms and AMH serum level can predict assisted reproduction outcomes: a cross-sectional study, Cell Physiol Biochem., 35, 1401, 10.1159/000373961 · doi:10.1159/000373961
- Chang, 2018, Polycystic ovary syndrome and hyperandrogenic states, 520
- Rosencrantz, 2010, Comparison of inhibin B and estradiol responses to intravenous FSH in women with polycystic ovary syndrome and normal women, Hum Reprod., 25, 198, 10.1093/humrep/dep373 · doi:10.1093/humrep/dep373
- Dray, 2018, Mismatch repair gene mutations lead to lynch syndrome colorectal cancer in rhesus macaques, Genes Cancer., 9, 142, 10.18632/genesandcancer.170 · doi:10.18632/genesandcancer.170
- Garcia-Rudaz, 2011, Excessive ovarian production of nerve growth factor elicits granulosa cell apoptosis by setting in motion a tumor necrosis factor α/stathmin-mediated death signaling pathway, Reproduction., 142, 319, 10.1530/REP-11-0134 · doi:10.1530/rep-11-0134
Cited by
Joham, A. E., Norman, R. J., Stener-Victorin, E., Legro, R. S., Franks, S., Moran, L. J., Boyle, J., & Teede, H. J. (2022) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(22)00163-2 · Cited by 838
Self-citationUpdate on PCOS: consequences, challenges, and guiding treatment
Hoeger, K. M., Dokras, A., & Piltonen, T. (2021) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgaa839 · Cited by 610
Deconstructing a Syndrome: Genomic Insights Into PCOS Causal Mechanisms and Classification
Dapas, M., & Dunaif, A. (2022) · Endocrine Reviews · doi:10.1210/endrev/bnac001 · Cited by 300
Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment
parker, J., O'Brien, C., Hawrelak, J., & Gersh, F. (2021) · doi:10.20944/preprints202112.0088.v1 · Cited by 113
Polycystic Ovary Syndrome: An Evolutionary Adaptation to Lifestyle and the Environment
Parker, J., O’Brien, C., Hawrelak, J., & Gersh, F. L. (2022) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph19031336 · Cited by 114
“Experimental studies in primates, sheep, rats and mice show that PCOS-like syndromes can be induced by a range of treatments including androgens, anti-Mullerian hormone and letrozole [19,44,46].”
Background
Metadata
- Authors
- Stener-Victorin, E., Padmanabhan, V., Walters, K. A., Campbell, R. E., Benrick, A., Giacobini, P., Dumesic, D. A., & Abbott, D. H.
- Venue
- Endocrine Reviews
- Publisher
- The Endocrine Society
- Published
- 2020-04-20
- Volume
- 41
- Issue
- 4
- ISSN
- 0163-769X (ISSN-L)
- 1945-7189
- OpenAlex
- W3016682625
- Cited by
- 348
- References
- 359
- FWCI
- 32.01
- Type
- journal article
- Language
- en
- Open access
- hybrid
- Funders
- Swedish Medical Research Council (2018-02435)
- Novo Nordisk Foundation (NNF19OC0056647)
- Stockholm County Council and Karolinska Institutet
- National Institutes of Health (HD041098, HD044232, P50HD071836, HD044405, HD028934, OD011106, DK121559)
- European Research Council (ERC-2016-CoG, 725149/REPRODAMH)
- National Health and Medical Research Council (APP1022648, APP1158540)
- Health Research Council of New Zealand (18-671)
- Royal Society Marsden Fund (17-64)
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- Stener-Victorin, E., Padmanabhan, V., Walters, K. A., Campbell, R. E., Benrick, A., Giacobini, P., Dumesic, D. A., & Abbott, D. H. (2020). Animal Models to Understand the Etiology and Pathophysiology of Polycystic Ovary Syndrome. Endocrine Reviews. https://doi.org/10.1210/endrev/bnaa010
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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