Detection of Parental Contribution to Molar Genome Leads to Diagnosis of Recurrent Hydatidiform Mole in a Family with <i>NLRP7</i> Variants

Wang, Rong-Yue; Li, Yujuan; Li, Zhen; Jiang, Fan; Gu, Congmin; Li, Dong-Zhi

doi:10.1080/15513815.2020.1852463

Cited by 1 publication

(1 citation statement)

References 12 publications

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“…Finally, Abi Nahed et al recently demonstrated that the activation of the NLRP7 inflammasome in a trophoblastic cell line induced the secretion of IL1β but not IL18 [ 150 ]. Numerous studies have described the involvement of the NLRP7 inflammasome in some obstetrical complications, such as the recurrent hydatidiform mole (a disease characterized by an excessive trophoblastic proliferation without embryonic development), especially those related to mutations of NLRP7 [ 151 , 152 , 153 , 154 , 155 ]. In addition, the NLRP7 inflammasome is highly expressed by placental trophoblast cells and is deregulated in fetal growth restrictions, a disorder importantly related to abnormal placental development [ 150 ].…”

Section: Inflammasomesmentioning

confidence: 99%

Pathophysiological Implication of Pattern Recognition Receptors in Fetal Membranes Rupture: RAGE and NLRP Inflammasome

et al. 2021

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Preterm prelabor ruptures of fetal membranes (pPROM) are a pregnancy complication responsible for 30% of all preterm births. This pathology currently appears more as a consequence of early and uncontrolled process runaway activation, which is usually implicated in the physiologic rupture at term: inflammation. This phenomenon can be septic but also sterile. In this latter case, the inflammation depends on some specific molecules called “alarmins” or “damage-associated molecular patterns” (DAMPs) that are recognized by pattern recognition receptors (PRRs), leading to a microbial-free inflammatory response. Recent data clarify how this activation works and which receptor translates this inflammatory signaling into fetal membranes (FM) to manage a successful rupture after 37 weeks of gestation. In this context, this review focused on two PRRs: the receptor for advanced glycation end-products (RAGE) and the NLRP7 inflammasome.

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