کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
10736621 1045728 2013 26 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Pathogenesis of acute stroke and the role of inflammasomes
ترجمه فارسی عنوان
پاتوژنز سکته حاد و نقش التهاب لگن
کلمات کلیدی
التهاب سکته مغزی ایسکمیک، کاسپاز-1، سیتوکین ها، رفتار،
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی سالمندی
چکیده انگلیسی
Inflammation is an innate immune response to infection or tissue damage that is designed to limit harm to the host, but contributes significantly to ischemic brain injury following stroke. The inflammatory response is initiated by the detection of acute damage via extracellular and intracellular pattern recognition receptors, which respond to conserved microbial structures, termed pathogen-associated molecular patterns or host-derived danger signals termed damage-associated molecular patterns. Multi-protein complexes known as inflammasomes (e.g. containing NLRP1, NLRP2, NLRP3, NLRP6, NLRP7, NLRP12, NLRC4, AIM2 and/or Pyrin), then process these signals to trigger an effector response. Briefly, signaling through NLRP1 and NLRP3 inflammasomes produces cleaved caspase-1, which cleaves both pro-IL-1β and pro-IL-18 into their biologically active mature pro-inflammatory cytokines that are released into the extracellular environment. This review will describe the molecular structure, cellular signaling pathways and current evidence for inflammasome activation following cerebral ischemia, and the potential for future treatments for stroke that may involve targeting inflammasome formation or its products in the ischemic brain.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Ageing Research Reviews - Volume 12, Issue 4, September 2013, Pages 941-966
نویسندگان
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