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S100A8/A9在脓毒症和脓毒症相关器官损伤中的研究进展
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Abstract:
脓毒症是重症监护病房患者死亡的首要原因，它是由入侵感染引起的不受控制的全身反应引起的，导致多个器官和系统的广泛损害。最近，S100A8/A9已成为脓毒症和脓毒症诱导的器官损伤的一种有前景的生物标志物，靶向S100A8/A9似乎可以改善炎症诱导的组织损伤并改善不良结局。S100A8/A9是一种钙结合异二聚体，主要存在于中性粒细胞和单核细胞中，是一种具有促炎和免疫抑制特性的致病分子，在脓毒症的发病机制中至关重要。因此，提高我们对S100A8/A9在脓毒症发展中的病理作用机制的理解，对于推进脓毒症的研究至关重要。本综述讨论了S100A8/A9的生物学特性及其释放机制，总结了S100A8/A9在脓毒症及其相关器官损伤中的重要作用的最新进展，并强调了其作为脓毒症诊断生物标志物和治疗靶点的潜力。
Sepsis, the leading cause of death in intensive care unit patients, is caused by an uncontrolled systemic reaction caused by an invasive infection, resulting in widespread damage to multiple organs and systems. Recently, S100A8/A9 has emerged as a promising biomarker for sepsis and sepsis-induced organ damage, and targeting S100A8/A9 appears to ameliorate inflammation-induced tissue damage and improve poor outcomes. S100A8/A9, a calcium-bound heterodimer predominantly found in neutrophils and monocytes, is a pathogenic molecule with pro-inflammatory and immunosuppressive properties that is critical in the pathogenesis of sepsis. Therefore, improving our understanding of the pathological mechanism of S100A8/A9 in the development of sepsis is essential to advance the research of sepsis. This review discusses the biology of S100A8/A9 and its release mechanism, summarizes recent advances in the important role of S100A8/A9 in sepsis and its associated organ damage, and highlights its potential as a diagnostic biomarker and therapeutic target for sepsis.
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