Jennekens Jitte, Braithwaite Sue A, Luijk Bart, van der Kaaij Niels P, Vrisekoop Nienke, de Jager Saskia C A, de Heer Linda M
Department of Cardiothoracic Surgery, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands.
Department of Anesthesiology, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands.
Int J Mol Sci. 2025 Jul 15;26(14):6776. doi: 10.3390/ijms26146776.
Primary graft dysfunction (PGD) remains a major complication after lung transplantation. Donor lung ischemia followed by reperfusion drives oxidative stress and inflammatory responses. The pathophysiology is influenced by various donor-, procedure-, and recipient-related factors, which complicates the identification of biomarkers for evaluation of donor lung injury or therapeutic interventions to minimize PGD. This review provides an overview of the molecular pathways that contribute to PGD pathophysiology, including those involved in loss of endothelial-epithelial membrane integrity, neutrophil infiltration, and the development of pulmonary edema.
原发性移植肺功能障碍(PGD)仍然是肺移植后的主要并发症。供体肺缺血后再灌注会引发氧化应激和炎症反应。其病理生理学受到多种与供体、手术和受体相关因素的影响,这使得鉴定用于评估供体肺损伤的生物标志物或用于将PGD降至最低的治疗干预措施变得复杂。本综述概述了导致PGD病理生理学的分子途径,包括那些与内皮-上皮膜完整性丧失、中性粒细胞浸润和肺水肿发展有关的途径。