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首页> 外文期刊>Endocrine, metabolic & immune disorders drug targets >One Special Question to Start with: Can HIF/NFkB be a Target in Inflammation?
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One Special Question to Start with: Can HIF/NFkB be a Target in Inflammation?

机译:首先要提出一个特殊问题:HIF / NFkB能否成为炎症的靶标?

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摘要

Hypoxia and Inflammation are strictly interconnected with important consequences at clinical and therapeutic level. While cell and tissue damage due to acute hypoxia mostly leads to cell necrosis, in chronic hypoxia, cells that are located closer to vessels are able to survive adapting their phenotype through the expression of a number of genes, including proinflammatory receptors for alarmins. These receptors are activated by alarmins released by necrotic cells and generate signals for master transcription factors such as NFkB, AP1, etc. which control hundreds of genes for innate immunity and damage repair. Clinical consequences of chronic inflammatory reparative response activation include cell and tissue remodeling, damage in the primary site and, the systemic involvement of distant organs and tissues.
机译:缺氧和炎症与临床和治疗水平上的重要后果密切相关。虽然急性缺氧引起的细胞和组织损伤主要导致细胞坏死,但在慢性缺氧中,靠近血管的细胞能够通过表达多种基因(包括警报蛋白的促炎性受体)表达适应表型。这些受体被坏死细胞释放的警报蛋白激活,并为诸如NFkB,AP1等的主转录因子生成信号,这些转录因子控制数百种基因以进行先天免疫和损伤修复。慢性炎症修复反应激活的临床后果包括细胞和组织重塑,原发部位损伤以及远处器官和组织的全身性受累。

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