医学
背景(考古学)
临床试验
重症监护医学
生物信息学
相关性(法律)
临床意义
糖尿病
协调
心理干预
病理
生物
内分泌学
法学
古生物学
政治学
物理
精神科
声学
作者
Anupam Agarwal,Zheng Dong,Raymond C. Harris,Patrick Murray,Samir M. Parikh,Mitchell H. Rosner,John A. Kellum,Claudio Ronco
出处
期刊:Journal of The American Society of Nephrology
日期:2016-02-09
卷期号:27 (5): 1288-1299
被引量:189
标识
DOI:10.1681/asn.2015070740
摘要
In this article, we review the current evidence for the cellular and molecular mechanisms of AKI, focusing on epithelial cell pathobiology and related cell-cell interactions, using ischemic AKI as a model. Highlighted are the clinical relevance of cellular and molecular targets that have been investigated in experimental models of ischemic AKI and how such models might be improved to optimize translation into successful clinical trials. In particular, development of more context-specific animal models with greater relevance to human AKI is urgently needed. Comorbidities that could alter patient susceptibility to AKI, such as underlying diabetes, aging, obesity, cancer, and CKD, should also be considered in developing these models. Finally, harmonization between academia and industry for more clinically relevant preclinical testing of potential therapeutic targets and better translational clinical trial design is also needed to achieve the goal of developing effective interventions for AKI.
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