A Possible Mechanism of Renal Cell Death after Ischemia/reperfusion

In this issue of Kidney International, Linkermann, et al. provide the first evidence for a possible biochemical mechanism of necrotic kidney cell death associated with renal ischemia/reperfusion-induced acute kidney injury. The mechanisms of several pathways resulting in programmed necrosis were rec...

Descripción completa

Detalles Bibliográficos
Autores principales: Price, Peter M., Hodeify, Rawad
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2012
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3324283/
https://www.ncbi.nlm.nih.gov/pubmed/22460652
http://dx.doi.org/10.1038/ki.2011.495
_version_ 1782229293052461056
author Price, Peter M.
Hodeify, Rawad
author_facet Price, Peter M.
Hodeify, Rawad
author_sort Price, Peter M.
collection PubMed
description In this issue of Kidney International, Linkermann, et al. provide the first evidence for a possible biochemical mechanism of necrotic kidney cell death associated with renal ischemia/reperfusion-induced acute kidney injury. The mechanisms of several pathways resulting in programmed necrosis were recently elucidated and rely on receptor-interacting protein kinases 1 and 3. Using an inhibitor of one of these kinases, Linkermann was able to ameliorate functional and morphologic kidney damage after ischemia/reperfusion.
format Online
Article
Text
id pubmed-3324283
institution National Center for Biotechnology Information
language English
publishDate 2012
record_format MEDLINE/PubMed
spelling pubmed-33242832012-10-01 A Possible Mechanism of Renal Cell Death after Ischemia/reperfusion Price, Peter M. Hodeify, Rawad Kidney Int Article In this issue of Kidney International, Linkermann, et al. provide the first evidence for a possible biochemical mechanism of necrotic kidney cell death associated with renal ischemia/reperfusion-induced acute kidney injury. The mechanisms of several pathways resulting in programmed necrosis were recently elucidated and rely on receptor-interacting protein kinases 1 and 3. Using an inhibitor of one of these kinases, Linkermann was able to ameliorate functional and morphologic kidney damage after ischemia/reperfusion. 2012-04 /pmc/articles/PMC3324283/ /pubmed/22460652 http://dx.doi.org/10.1038/ki.2011.495 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
Price, Peter M.
Hodeify, Rawad
A Possible Mechanism of Renal Cell Death after Ischemia/reperfusion
title A Possible Mechanism of Renal Cell Death after Ischemia/reperfusion
title_full A Possible Mechanism of Renal Cell Death after Ischemia/reperfusion
title_fullStr A Possible Mechanism of Renal Cell Death after Ischemia/reperfusion
title_full_unstemmed A Possible Mechanism of Renal Cell Death after Ischemia/reperfusion
title_short A Possible Mechanism of Renal Cell Death after Ischemia/reperfusion
title_sort possible mechanism of renal cell death after ischemia/reperfusion
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3324283/
https://www.ncbi.nlm.nih.gov/pubmed/22460652
http://dx.doi.org/10.1038/ki.2011.495
work_keys_str_mv AT pricepeterm apossiblemechanismofrenalcelldeathafterischemiareperfusion
AT hodeifyrawad apossiblemechanismofrenalcelldeathafterischemiareperfusion
AT pricepeterm possiblemechanismofrenalcelldeathafterischemiareperfusion
AT hodeifyrawad possiblemechanismofrenalcelldeathafterischemiareperfusion

Ejemplares similares