Liu Shan
School of Medicine, South China University of Technology , Guangzhou , China.
Am J Physiol Renal Physiol. 2019 May 1;316(5):F974-F985. doi: 10.1152/ajprenal.00624.2017. Epub 2019 Mar 6.
Pathological changes in the heart or kidney can instigate the release of a cascade of cardiorenal mediators that promote injury in the other organ. Combined dysfunction of heart and kidney is referred to as cardiorenal syndrome (CRS) and has gained considerable attention. CRS has been classified into five distinct entities, each with different major pathophysiological changes. Despite the magnitude of the public health problem of CRS, the underlying mechanisms are incompletely understood, and effective intervention is unavailable. Animal models have allowed us to discover pathogenic molecular changes to clarify the pathophysiological mechanisms responsible for heart-kidney interactions and to enable more accurate risk stratification and effective intervention. Here, this article focuses on the use of currently available animal models to elucidate mechanistic insights in the clinical cardiorenal phenotype arising from primary cardiac injury, primary renal disease with special emphasis of chronic kidney disease-specific risk factors, and simultaneous cardiorenal/renocardiac dysfunction. The development of novel animal models that recapitulate more closely the cardiorenal phenotype in a clinical scenario and discover the molecular basis of this condition will be of great benefit.
心脏或肾脏的病理变化可促使一系列心肾介质的释放，这些介质会加重另一器官的损伤。心肾联合功能障碍被称为心肾综合征（CRS），已引起广泛关注。CRS已被分为五个不同类型，每种类型都有不同的主要病理生理变化。尽管CRS是一个严重的公共卫生问题，但其潜在机制尚未完全明确，且缺乏有效的干预措施。动物模型使我们能够发现致病的分子变化，以阐明心肾相互作用的病理生理机制，并实现更准确的风险分层和有效干预。本文重点介绍如何利用现有的动物模型，来阐明由原发性心脏损伤、原发性肾脏疾病（特别强调慢性肾病的特定危险因素）以及同时存在的心肾/肾心功能障碍所导致的临床心肾表型的机制。开发更能在临床情况下模拟心肾表型并发现该病症分子基础的新型动物模型将大有裨益。
