Fetal programming theory: Implication for the understanding of endometriosis
Human Immunology, ISSN: 0198-8859, Vol: 75, Issue: 3, Page: 208-217
2014
- 28Citations
- 50Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations28
- Citation Indexes28
- 28
- CrossRef21
- Captures50
- Readers50
- 50
Review Description
Comparison of the transcriptomes and proteomes of the decidualization-specific genes that express high vs low levels of the eutopic and ectopic endometrium of women with endometriosis compared with controls, could be useful in understanding the pathogenesis of endometriosis. Genome-wide comparison between decidual tissue and non-decidual tissue identified many genes significantly modulated in the process of decidualization. Comparison of eutopic endometrium and endometriotic sites also revealed up- and down-regulated genes. A combined analysis of the experimental data showed specific genes up-regulated both at the endometriotic site and in the decidualization process, representing a broad diversity of molecular functions, including cell cycle regulation, angiogenesis and adhesion molecules. In contrast, down-regulated genes identified in endometriosis among genes overexpressed in decidualization encode Müllerian embryogenesis, which includes transcription factors, hormonal regulation and cytokine expression. The mechanism responsible for insufficient decidualization in endometriosis may be mediated through down-regulation of the Müllerian embryogenesis-related genes. In conclusion, a range of decidualization resistance has been associated with endometriosis. Future study will identify the putative mechanisms relating epigenetic changes of decidualization susceptibility genes in early life to the risk of developing endometriosis in adulthood.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S019888591300606X; http://dx.doi.org/10.1016/j.humimm.2013.12.012; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84893772729&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/24374047; https://linkinghub.elsevier.com/retrieve/pii/S019888591300606X; https://dx.doi.org/10.1016/j.humimm.2013.12.012
Elsevier BV
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