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Pathogenesis of the systemic inflammatory syndrome and acute lung injury: role of iron mobilization and decompartmentalization

机译:全身炎症综合征和急性肺损伤的发病机制:铁动员和分解的作用

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First published November 30, 2007; doi:10.1152/ajplung.00169.2007.-Changes in iron homeostatic responses routinely accompany infectious or proinflammatory insults. The systemic inflammatory response syndrome (SIRS) and the development of acute lung injury (ALI) feature pronounced systemic and lung-specific alterations in iron/heme mobilization and decompartmentalization; such responses may be of pathological significance for both the onset and progression of acute inflammation. The potential for excessive iron-catalyzed oxidative stress, altered proinflammatory redox signaling, and provision of iron as a microbial growth factor represent obvious adverse aspects of altered in vivo iron handling. The release of hemoglobin during hemolytic disease or surgical procedures such as those utilizing cardiopulmonary bypass procedures further impacts on iron mobilization, turnover, and storage with associated implications. Genetic predisposition may ultimately determine the extent to which SIRS and related syndromes develop in response to such changes. The design of specific therapeutic interventions based on endogenous stratagems to limit adverse aspects of altered iron handling may prove of therapeutic benefit for the treatment of SIRS and ALI.fan J Physiol Lung Cell Mol Physiol 294: L16I-L174,
机译:2007年11月30日第一次出版; DOI:10.1152 / AJPLUNG.00169.2007.铁稳态反应的变化常规伴随着传染病或促炎侮辱。全身炎症反应综合征(SIRS)和急性肺损伤(ALI)的发育特征在于铁/血液动员和分解的系统和肺部特异性改变;这些反应可能对急性炎症的发作和进展具有病理意义。过量铁催化氧化应激的可能性,改变的促炎氧化还原信号传导,以及作为微生物生长因子的提供提供铁,代表了体内铁处理中改变的明显不利方面。在溶血性疾病或外科手术期间释放血红蛋白,例如利用心肺旁路程序的血栓制程序进一步影响铁的动员,周转和储存与相关的影响。遗传易感性最终可能最终确定主题患者和相关综合症的程度如何响应于这些变化而发展。基于内源性划分的特定治疗干预措施来限制改变的铁处理的不良方面,可以证明治疗SIRS和Ali.fan J Physiol肺细胞Mol Physiol 294:L16i-L174,

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