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急性肺损伤与修复过程中死细胞清除的最新进展

Recent advances in dead cell clearance during acute lung injury and repair.

作者信息

Noone Patrick M, Reddy Sekhar P

机构信息

Department of Pediatrics, College of Medicine, University of Illinois at Chicago, IL 60612, USA.

Department of Pathology, College of Medicine, University of Illinois at Chicago, IL 60612, USA.

出版信息

Fac Rev. 2021 Mar 30;10:33. doi: 10.12703/r/10-33. eCollection 2021.

Abstract

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are clinical syndromes that cause significant mortality in clinical settings and morbidity among survivors accompanied by huge healthcare costs. Lung-resident cell dysfunction/death and neutrophil alveolitis accompanied by proteinous edema are the main pathological features of ALI/ARDS. While understanding of the mechanisms underlying ALI/ARDS pathogenesis is progressing and potential treatments such as statin therapy, nutritional strategies, and mesenchymal cell therapy are emerging, poor clinical outcomes in ALI/ARDS patients persist. Thus, a better understanding of lung-resident cell death and neutrophil alveolitis and their mitigation and clearance mechanisms may provide new therapeutic strategies to accelerate lung repair and improve outcomes in critically ill patients. Macrophages are required for normal tissue development and homeostasis as well as regulating tissue injury and repair through modulation of inflammation and other cellular processes. While macrophages mediate various functions, here we review recent dead cell clearance (efferocytosis) mechanisms mediated by these immune cells for maintaining tissue homeostasis after infectious and non-infectious lung injury.

摘要

急性肺损伤(ALI)和急性呼吸窘迫综合征(ARDS)是临床综合征,在临床环境中会导致显著的死亡率,在幸存者中会引发疾病,同时伴有巨大的医疗成本。肺驻留细胞功能障碍/死亡以及伴有蛋白性水肿的中性粒细胞肺泡炎是ALI/ARDS的主要病理特征。虽然对ALI/ARDS发病机制的理解在不断进步,他汀类药物治疗、营养策略和间充质细胞治疗等潜在治疗方法也不断涌现,但ALI/ARDS患者的临床预后仍然很差。因此,更好地理解肺驻留细胞死亡和中性粒细胞肺泡炎及其缓解和清除机制,可能会提供新的治疗策略,以加速肺修复并改善重症患者的预后。巨噬细胞对于正常组织发育和稳态是必需的,并且通过调节炎症和其他细胞过程来调节组织损伤和修复。虽然巨噬细胞介导多种功能,但在此我们综述这些免疫细胞介导的最近的死细胞清除(吞噬作用)机制,以在感染性和非感染性肺损伤后维持组织稳态。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a70/8103909/678ddce5ae3e/facrev-10-33-g001.jpg

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