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      Cellular and Molecular Mechanisms of AKI

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          Abstract

          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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          Author and article information

          Journal
          J Am Soc Nephrol
          J. Am. Soc. Nephrol
          jnephrol
          jnephrol
          ASN
          Journal of the American Society of Nephrology : JASN
          American Society of Nephrology
          1046-6673
          1533-3450
          May 2016
          9 February 2016
          : 27
          : 5
          : 1288-1299
          Affiliations
          [* ]Division of Nephrology, and Nephrology Research and Training Center, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama;
          []Department of Cellular Biology and Anatomy, Georgia Regents University, Augusta, Georgia;
          []Division of Nephrology, Department of Medicine, Vanderbilt University, Nashville, Tennessee;
          [§ ]Department of Medicine, University College of Dublin, Dublin, Ireland;
          []Division of Nephrology and Center for Vascular Biology Research, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts;
          []Department of Medicine, Nephrology Division, and the Center for Immunity, Inflammation, and Regenerative Medicine, University of Virginia, Charlottesville, Virginia;
          [** ]Center for Critical Care Nephrology, Clinical Research, Investigation and Systems Modeling of Acute Illness Center, Department of Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; and
          [†† ]Department of Nephrology, Dialysis, and Transplantation, San Bortolo Hospital, and the International Renal Research Institute, 36100 Vicenza, Italy
          Author notes
          Correspondence: Dr. Anupam Agarwal, Director, Division of Nephrology, University of Alabama at Birmingham, 1900 University Boulevard, Tinsley Harrison Tower 647, Birmingham, AL 35294. Email: Agarwal@ 123456uab.edu
          Article
          PMC4849836 PMC4849836 4849836 2015070740
          10.1681/ASN.2015070740
          4849836
          26860342
          7eb75fce-7fb1-4cf0-a789-bddc9843a1fc
          Copyright © 2016 by the American Society of Nephrology
          History
          Page count
          Figures: 2, Tables: 0, Equations: 0, References: 115, Pages: 12
          Categories
          Up Front Matters
          Special Articles
          Custom metadata
          May 2016

          acute renal failure,kidney,pathophysiology of renal disease and progression

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