Dos Santos Claudia C
Interdepartmental Division of Critical Care, University of Toronto, 30, Bond Street 4-008, M5G 1W8, Toronto, Ontario, Canada.
Intensive Care Med. 2008 Apr;34(4):619-30. doi: 10.1007/s00134-007-0963-x. Epub 2008 Feb 9.
Acute respiratory distress syndrome (ARDS) is the most severe manifestation of acute lung injury (ALI). In patients who survive the acute injury the process of repair and remodelling may be an independent risk factor determining morbidity and mortality. This review explores recent advances in the field of fibroproliferative ARDS/ALI, with a special emphasis on (a) the primary contributing factors with a focus on cellular and soluble factors, and (b) mechanisms involved in repair and remodelling as they pertain to the importance of cell death, re-population, and matrix deposition.
Factors influencing progression to fibroproliferative ARDS vs. resolution and reconstitution of the normal pulmonary parenchymal architecture are poorly understood. Determinants of persistent injury and abnormal repair and remodelling may be profoundly affected by both environmental and genetic factors. Moreover, cumulative evidence suggests that acute inflammation and fibrosis may be in part independent and interactive processes that are autonomously regulated and thus amenable to individual and specific therapy.
Although our current understanding of these processes is limited by the inability to accurately replicate the complex human physiology in laboratory settings, it has recently become apparent that the process of repair and remodelling begins early in the course of ARDS/ALI and may be determined by the type of pulmonary injury. Understanding the mechanisms leading to and regulating fibroproliferative changes may contribute to the development of novel early therapeutic interventions in ARDS/ALI patients.
急性呼吸窘迫综合征（ARDS）是急性肺损伤（ALI）最严重的表现形式。在急性损伤中存活下来的患者，修复和重塑过程可能是决定发病率和死亡率的独立危险因素。本综述探讨了纤维增生性ARDS/ALI领域的最新进展，特别强调了：（a）主要促成因素，重点关注细胞和可溶性因子；（b）与细胞死亡、再增殖和基质沉积的重要性相关的修复和重塑机制。
对于影响进展为纤维增生性ARDS与正常肺实质结构的消退和重建的因素，我们了解甚少。持续损伤以及异常修复和重塑的决定因素可能受到环境和遗传因素的深刻影响。此外，越来越多的证据表明，急性炎症和纤维化可能在一定程度上是独立且相互作用的过程，它们自我调节，因此适合进行个体化和特异性治疗。
尽管我们目前对这些过程的理解受到无法在实验室环境中准确复制复杂人体生理学的限制，但最近已经很明显，修复和重塑过程在ARDS/ALI病程早期就已开始，并且可能由肺损伤的类型决定。了解导致和调节纤维增生性变化的机制可能有助于开发针对ARDS/ALI患者的新型早期治疗干预措施。
