2000
DOI: 10.1067/mob.2000.107330
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Programmed cell death (apoptosis) as a possible pathway to metalloproteinase activation and fetal membrane degradation in premature rupture of membranes

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Cited by 139 publications
(82 citation statements)
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“…Firstly, production and release of inflammatory cytokines may lead to increased prostaglandin secretion [5,12]. Secondly, pPROM and its consequence -preterm labour may be initiated by many factors such as infection, drugs or others [13]. There is also an evidence sup- Table 1.…”
Section: Discussionmentioning
confidence: 99%
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“…Firstly, production and release of inflammatory cytokines may lead to increased prostaglandin secretion [5,12]. Secondly, pPROM and its consequence -preterm labour may be initiated by many factors such as infection, drugs or others [13]. There is also an evidence sup- Table 1.…”
Section: Discussionmentioning
confidence: 99%
“…The role of MMPs in human labour and pPROM has been a subject of considerable study over the last decade. Increased collagenolysis, a drop in the collagen content of the membranes and activation of MMPs have been documented during active stage of labour [13][14][15][16].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Moore et al, 2009b;Menon et al, 2004;Zaga et al, 2004). Several groups have proposed the synergistic effects of MMP activation and apoptosis leading to rupture of the FM (McLaren et al, 2000a;Fortunato et al, 2000;Bowen et al, 2002;Lei et al, 1996). The promoter polymorphisms in some cytokines (TNF and IL-1 ) and MMPs (-1,-8,-9) have been identified to be associated with PPROM (Ferrand et al, 2002;Fujimoto et al, 2002;Hernandez-Guerrero et al, 2003;Roberts et al, 1999).…”
Section: Term Fm Develops a Para-cervical "Weak Zone" Where Rupture Imentioning
confidence: 99%
“…The causes of PTB are multiple, but intra-amniotic infection and chorioamnionitis are thought to be a major cause of spontaneous preterm labor (PTL) and preterm premature rupture of the fetal membranes (PPROM). Extensive data from the literature have reported mechanisms involving a feed-forward loop network in normal parturition, where proinflammatory cytokines are able to stimulate production of PGs and thereby uterine contractions and to upregulate matrix metalloproteinase (MMP) activation and programmed cell death (apoptosis), leading to the weakening and the rupture of the fetal membranes (2)(3)(4)(5).…”
mentioning
confidence: 99%