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NODding off AKI with Progranulin?
Inflammation is a common feature of murine models of AKI. The endogenous mechanisms which serve to limit inflammation and reduce the severity of AKI are poorly understood. Zhou et al identify progranulin as one such protective mediator. Deficiency of progranulin was associated with increased inflamm...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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2015
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4425217/ https://www.ncbi.nlm.nih.gov/pubmed/25951064 http://dx.doi.org/10.1038/ki.2015.14 |
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author | Tadagavadi, Raghu K. Reeves, W. Brian |
author_facet | Tadagavadi, Raghu K. Reeves, W. Brian |
author_sort | Tadagavadi, Raghu K. |
collection | PubMed |
description | Inflammation is a common feature of murine models of AKI. The endogenous mechanisms which serve to limit inflammation and reduce the severity of AKI are poorly understood. Zhou et al identify progranulin as one such protective mediator. Deficiency of progranulin was associated with increased inflammation and increased injury in both ischemic and nephrotoxic models of AKI. Moreover, administration of exogenous progranulin reduced AKI even when delivered after AKI was established. Interference in NOD2 pathways is suggested as a possible mechanism for protection. PRGN-based therapeutics are under development and might have application in the treatment or prevention of AKI. |
format | Online Article Text |
id | pubmed-4425217 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
record_format | MEDLINE/PubMed |
spelling | pubmed-44252172015-11-01 NODding off AKI with Progranulin? Tadagavadi, Raghu K. Reeves, W. Brian Kidney Int Article Inflammation is a common feature of murine models of AKI. The endogenous mechanisms which serve to limit inflammation and reduce the severity of AKI are poorly understood. Zhou et al identify progranulin as one such protective mediator. Deficiency of progranulin was associated with increased inflammation and increased injury in both ischemic and nephrotoxic models of AKI. Moreover, administration of exogenous progranulin reduced AKI even when delivered after AKI was established. Interference in NOD2 pathways is suggested as a possible mechanism for protection. PRGN-based therapeutics are under development and might have application in the treatment or prevention of AKI. 2015-05 /pmc/articles/PMC4425217/ /pubmed/25951064 http://dx.doi.org/10.1038/ki.2015.14 Text en http://www.nature.com/authors/editorial_policies/license.html#terms Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms |
spellingShingle | Article Tadagavadi, Raghu K. Reeves, W. Brian NODding off AKI with Progranulin? |
title | NODding off AKI with Progranulin? |
title_full | NODding off AKI with Progranulin? |
title_fullStr | NODding off AKI with Progranulin? |
title_full_unstemmed | NODding off AKI with Progranulin? |
title_short | NODding off AKI with Progranulin? |
title_sort | nodding off aki with progranulin? |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4425217/ https://www.ncbi.nlm.nih.gov/pubmed/25951064 http://dx.doi.org/10.1038/ki.2015.14 |
work_keys_str_mv | AT tadagavadiraghuk noddingoffakiwithprogranulin AT reeveswbrian noddingoffakiwithprogranulin |