دانلود مقاله ISI انگلیسی شماره 141561
ترجمه فارسی عنوان مقاله

هموستاز پلاسبا و التهاب استریل: بینش جدید به بیماری عروق بارداری

عنوان انگلیسی
Placental hemostasis and sterile inflammation: New insights into gestational vascular disease
کد مقاله سال انتشار تعداد صفحات مقاله انگلیسی
141561 2017 4 صفحه PDF
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Thrombosis Research, Volume 151, Supplement 1, March 2017, Pages S30-S33

ترجمه کلمات کلیدی
بیماری عروق حاملگی، عوارض ناشی از قطعه قطعه پلاکت ها، التهاب درجه پایین درمان ضدالتهاب،
کلمات کلیدی انگلیسی
Gestational vascular disease; Placenta-mediated complications; Platelets; Low-grade inflammation; Antiplatelet therapy;
پیش نمایش مقاله
پیش نمایش مقاله  هموستاز پلاسبا و التهاب استریل: بینش جدید به بیماری عروق بارداری

چکیده انگلیسی

Activation of the coagulation and inflammatory systems are physiologically occurring during pregnancy. However, excess activation of either system is well documented in gestational vascular diseases (GVD). GVD are placenta-mediated pregnancy complications and a major cause of feto-maternal morbidity and mortality. The causal relevance of excess coagulation and inflammatory responses for GVD remains largely unknown. Deciphering the causal relationship of excess coagulation and inflammation in GVD may allow conceptualizing new therapeutic approaches to combat GVD. Platelet activation and procoagulant extracellular vesicles (EVs) provide a link between coagulation and inflammation and their activation or generation in GVD is well established. As recently shown EVs cause sterile placental inflammation by activating maternal platelets that release ATP and activate purinergic receptor signaling and NLRP3 inflammasome in the embryonic trophoblast. This thrombo-inflammatory mechanism suggests a novel link between coagulation activation and sterile inflammation in GVD. These findings highlight a role of anti-platelet therapies in GVD. In addition, targeting the inflammasome alone or in combination with platelet inhibition may provide a new therapeutic strategy in GVD.