FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2126195456> ?p ?o ?g. }

• W2126195456 endingPage "557" @default.
• W2126195456 startingPage "542" @default.
• W2126195456 abstract "BACKGROUND Mechanisms underlying early reproductive loss in the human are beginning to be elucidated. The migratory and invasive capacity of human endometrial stromal cells (ESCs) is increasingly recognized to contribute to the intense tissue remodelling associated with embryo implantation, trophoblast invasion and endometrial regeneration. In this review, we examine the signals and mechanisms that control ESC migration and invasion and assess how deregulation of these cell functions contributes to common reproductive disorders. METHODS The PubMed database was searched for publications on motility and invasiveness of human ESCs in normal endometrial function and in reproductive disorders including implantation failure, recurrent pregnancy loss (RPL), endometriosis and adenomyosis, covering the period 2000-2012. RESULTS Increasing evidence suggests that implantation failure and RPL involve abnormal migratory responses of decidualizing ESCs to embryo and trophoblast signals. Numerous reports indicate that endometriosis, as well as adenomyosis, is associated with increased basal and stimulated invasiveness of ESCs and their progenitor cells, suggesting a link between a heightened menstrual repair response and the formation of ectopic implants. Migration and invasiveness of ESCs are controlled by a complex array of hormones, growth factors, chemokines and inflammatory mediators, and involve signalling through Rho GTPases, phosphatidylinositol-3-kinase and mitogen-activated protein kinase pathways. CONCLUSIONS Novel concepts are extending our understanding of the key functions of ESCs in effecting tissue repair imposed by cyclic menstruation and parturition. Migration of decidualizing ESCs also serves to support blastocyst implantation and embryo selection through discriminate motile responses directed by embryo quality. Targeting regulatory molecules holds promise for developing new strategies for the treatment of reproductive disorders such as endometriosis and recurrent miscarriage; and harnessing the migratory capacity of progenitor mesenchymal stem cells in the endometrium may offer new opportunities in regenerative medicine." @default.
• W2126195456 created "2016-06-24" @default.
• W2126195456 creator A5023237739 @default.
• W2126195456 creator A5025845183 @default.
• W2126195456 creator A5028455936 @default.
• W2126195456 creator A5079813676 @default.
• W2126195456 creator A5091306061 @default.
• W2126195456 date "2013-07-04" @default.
• W2126195456 modified "2023-09-30" @default.
• W2126195456 title "The motile and invasive capacity of human endometrial stromal cells: implications for normal and impaired reproductive function" @default.
• W2126195456 cites W1489869710 @default.
• W2126195456 cites W1602718081 @default.
• W2126195456 cites W1964585044 @default.
• W2126195456 cites W1967265143 @default.
• W2126195456 cites W1967734600 @default.
• W2126195456 cites W1969397621 @default.
• W2126195456 cites W1969979700 @default.
• W2126195456 cites W1972693751 @default.
• W2126195456 cites W1974272339 @default.
• W2126195456 cites W1975047209 @default.
• W2126195456 cites W1979277919 @default.
• W2126195456 cites W1979762429 @default.
• W2126195456 cites W1990329963 @default.
• W2126195456 cites W1990332775 @default.
• W2126195456 cites W1990389515 @default.
• W2126195456 cites W1992079665 @default.
• W2126195456 cites W1993866784 @default.
• W2126195456 cites W2001634461 @default.
• W2126195456 cites W2002449811 @default.
• W2126195456 cites W2005487987 @default.
• W2126195456 cites W2007059239 @default.
• W2126195456 cites W2011053249 @default.
• W2126195456 cites W2015679500 @default.
• W2126195456 cites W2016417330 @default.
• W2126195456 cites W2020433921 @default.
• W2126195456 cites W2020676269 @default.
• W2126195456 cites W2024411072 @default.
• W2126195456 cites W2029933078 @default.
• W2126195456 cites W2033126075 @default.
• W2126195456 cites W2033389118 @default.
• W2126195456 cites W2034817882 @default.
• W2126195456 cites W2040105042 @default.
• W2126195456 cites W2041847148 @default.
• W2126195456 cites W2044895919 @default.
• W2126195456 cites W2045461902 @default.
• W2126195456 cites W2045739383 @default.
• W2126195456 cites W2047682029 @default.
• W2126195456 cites W2049014099 @default.
• W2126195456 cites W2049222017 @default.
• W2126195456 cites W2049230776 @default.
• W2126195456 cites W2050435980 @default.
• W2126195456 cites W2053301892 @default.
• W2126195456 cites W2053701919 @default.
• W2126195456 cites W2058177024 @default.
• W2126195456 cites W2065346340 @default.
• W2126195456 cites W2066873624 @default.
• W2126195456 cites W2071667212 @default.
• W2126195456 cites W2071883174 @default.
• W2126195456 cites W2072322981 @default.
• W2126195456 cites W2073882976 @default.
• W2126195456 cites W2074307523 @default.
• W2126195456 cites W2074682657 @default.
• W2126195456 cites W2075091190 @default.
• W2126195456 cites W2079375104 @default.
• W2126195456 cites W2082276924 @default.
• W2126195456 cites W2085996922 @default.
• W2126195456 cites W2086641174 @default.
• W2126195456 cites W2090986875 @default.
• W2126195456 cites W2091581681 @default.
• W2126195456 cites W2092182760 @default.
• W2126195456 cites W2093060517 @default.
• W2126195456 cites W2094943622 @default.
• W2126195456 cites W2095115481 @default.
• W2126195456 cites W2096282446 @default.
• W2126195456 cites W2096674085 @default.
• W2126195456 cites W2100488321 @default.
• W2126195456 cites W2101519077 @default.
• W2126195456 cites W2102312968 @default.
• W2126195456 cites W2102675401 @default.
• W2126195456 cites W2104784251 @default.
• W2126195456 cites W2106020828 @default.
• W2126195456 cites W2106489014 @default.
• W2126195456 cites W2106578670 @default.
• W2126195456 cites W2106927311 @default.
• W2126195456 cites W2108649673 @default.
• W2126195456 cites W2109191430 @default.
• W2126195456 cites W2110789099 @default.
• W2126195456 cites W2111141200 @default.
• W2126195456 cites W2111676688 @default.
• W2126195456 cites W2111937306 @default.
• W2126195456 cites W2112668385 @default.
• W2126195456 cites W2112675387 @default.
• W2126195456 cites W2113723296 @default.
• W2126195456 cites W2113849764 @default.
• W2126195456 cites W2115476730 @default.
• W2126195456 cites W2115523693 @default.
• W2126195456 cites W2115668011 @default.
• W2126195456 cites W2118043562 @default.

• next