Hypothesis: inhibition of endothelium-derived relaxing factor by haemoglobin in the pathogenesis of pre-eclampsia
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Circular RNA expression profiling identifies hsa_circ_0011460 as a novel molecule in severe preeclampsia
2019, Pregnancy HypertensionCitation Excerpt :This finding indirectly suggests that vasodilation and regulation of blood vessel size may be involved in the onset of PE. In addition, clinical studies [23,24] reported that maternal endothelial function and aberrant concentrations of the endogenous inhibitor of endothelial nitric oxide synthase (ADMA) were associated with PE. Huang et al. [25] reported that PE is associated with impaired maternal-foetal nutrient transfer, and the amino acid transporters SLC7A7 and SLC38A5 showed marked differences between controls and PE.
Is there a link between endothelial dysfunction, coagulation activation and nitric oxide synthesis in preeclampsia?
2013, Clinica Chimica ActaCitation Excerpt :NO could react rapidly with hemoglobin iron instead of the reaction between iron from guanylate cyclase. The inactivation of NO by hemoglobin iron in PE was previously raised by Sarrel et al. [38]. Second, several studies on women with PE suggested a relationship between enhanced O2− generation and endothelial injury, inflammation [39] as well as a decreased superoxide dismutase [40].
Circulating microparticles in severe preeclampsia
2012, Clinica Chimica ActaCitation Excerpt :Our data showed increased number of erythrocyte-derived MPs in women with severe PE. This finding could be explained by hemolysis, which is commonly observed in this disease [28]. Because fibrin clots have been observed in the microvasculature of women with PE, one hypothesis is that erythrocytes are lysed by colliding with such clots and result in MP release [29].
Increased circulating cell-free hemoglobin levels reduce nitric oxide bioavailability in preeclampsia
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2003, Clinical Neurology and NeurosurgeryBlood glutathione redox status in gestational hypertension
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