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血小板激活作为慢性阻塞性肺疾病动脉血栓形成风险的新机制。

Platelet activation as a novel mechanism of atherothrombotic risk in chronic obstructive pulmonary disease.

机构信息

Dipartimento di Medicina Interna--Az. Spedali Civili di Brescia e Università di Brescia.

出版信息

Expert Rev Hematol. 2013 Aug;6(4):475-83. doi: 10.1586/17474086.2013.814835.

Abstract

Chronic obstructive pulmonary disease (COPD) is characterized by pulmonary and systemic inflammation. In particular, the clinical course of this disease typically leads to periodic exacerbation involving inflammatory response and both respiratory and cardiovascular symptoms. Even though the exact mechanisms underlying the pathogenesis of COPD and its chronic and acute inflammation have not yet been fully understood, many studies have been highlighting the role of the endothelium, platelets (PTL) and other circulating blood cells. PLT are crucial for hemostasis and, once activated by a number of different factors, will mediate endothelium adhesion, and the rolling and activation of other circulating cells, such as neutrophils, which become a cause of tissue damage during the inflammatory process. The aim of this review is to highlight the onset of activation, thrombus formation and inflammatory amplification with particular regard to the COPD patients and the course of their acute exacerbations.

摘要

慢性阻塞性肺疾病(COPD)的特征是肺部和全身炎症。特别是,这种疾病的临床过程通常会导致周期性恶化,涉及炎症反应以及呼吸和心血管症状。尽管 COPD 的发病机制及其慢性和急性炎症的确切机制尚未完全了解,但许多研究已经强调了内皮细胞、血小板(PTL)和其他循环血细胞的作用。PLT 对于止血至关重要,一旦被许多不同的因素激活,它们将介导内皮细胞黏附以及其他循环细胞(如中性粒细胞)的滚动和激活,这些细胞在炎症过程中成为组织损伤的原因。本综述的目的是强调 COPD 患者及其急性恶化过程中激活、血栓形成和炎症放大的发生。

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