Nieuwenhuijs-Moeke Gertrude J, Pischke Søren E, Berger Stefan P, Sanders Jan Stephan F, Pol Robert A, Struys Michel M R F, Ploeg Rutger J, Leuvenink Henri G D
Department of Anesthesiology, University of Groningen, University Medical Centre Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands.
Clinic for Emergencies and Critical Care, Department of Anesthesiology, Department of Immunology, Oslo University Hospital, 4950 Nydalen, 0424 Oslo, Norway.
J Clin Med. 2020 Jan 17;9(1):253. doi: 10.3390/jcm9010253.
Ischemia and reperfusion injury (IRI) is a complex pathophysiological phenomenon, inevitable in kidney transplantation and one of the most important mechanisms for non- or delayed function immediately after transplantation. Long term, it is associated with acute rejection and chronic graft dysfunction due to interstitial fibrosis and tubular atrophy. Recently, more insight has been gained in the underlying molecular pathways and signalling cascades involved, which opens the door to new therapeutic opportunities aiming to reduce IRI and improve graft survival. This review systemically discusses the specific molecular pathways involved in the pathophysiology of IRI and highlights new therapeutic strategies targeting these pathways.
缺血再灌注损伤(IRI)是一种复杂的病理生理现象,在肾移植中不可避免,并且是移植后立即出现无功能或延迟功能的最重要机制之一。从长期来看,它与急性排斥反应以及因间质纤维化和肾小管萎缩导致的慢性移植肾功能障碍有关。最近,我们对其潜在的分子途径和信号级联反应有了更多了解,这为旨在减少IRI和提高移植肾存活率的新治疗机会打开了大门。本综述系统地讨论了IRI病理生理学中涉及的特定分子途径,并重点介绍了针对这些途径的新治疗策略。