| pubmed-article:15253693 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15253693 | lifeskim:mentions | umls-concept:C0012634 | lld:lifeskim |
| pubmed-article:15253693 | lifeskim:mentions | umls-concept:C0022660 | lld:lifeskim |
| pubmed-article:15253693 | lifeskim:mentions | umls-concept:C0475224 | lld:lifeskim |
| pubmed-article:15253693 | lifeskim:mentions | umls-concept:C0333348 | lld:lifeskim |
| pubmed-article:15253693 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:15253693 | pubmed:dateCreated | 2004-7-15 | lld:pubmed |
| pubmed-article:15253693 | pubmed:abstractText | Inflammation plays a major role in the pathophysiology of acute renal failure resulting from ischemia. In this review, we discuss the contribution of endothelial and epithelial cells and leukocytes to this inflammatory response. The roles of cytokines/chemokines in the injury and recovery phase are reviewed. The ability of the mouse kidney to be protected by prior exposure to ischemia or urinary tract obstruction is discussed as a potential model to emulate as we search for pharmacologic agents that will serve to protect the kidney against injury. Understanding the inflammatory response prevalent in ischemic kidney injury will facilitate identification of molecular targets for therapeutic intervention. | lld:pubmed |
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| pubmed-article:15253693 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15253693 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15253693 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15253693 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15253693 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15253693 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:15253693 | pubmed:issn | 0085-2538 | lld:pubmed |
| pubmed-article:15253693 | pubmed:author | pubmed-author:BonventreJose... | lld:pubmed |
| pubmed-article:15253693 | pubmed:author | pubmed-author:ZukAnnaA | lld:pubmed |
| pubmed-article:15253693 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15253693 | pubmed:volume | 66 | lld:pubmed |
| pubmed-article:15253693 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15253693 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15253693 | pubmed:pagination | 480-5 | lld:pubmed |
| pubmed-article:15253693 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
| pubmed-article:15253693 | pubmed:meshHeading | pubmed-meshheading:15253693... | lld:pubmed |
| pubmed-article:15253693 | pubmed:meshHeading | pubmed-meshheading:15253693... | lld:pubmed |
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| pubmed-article:15253693 | pubmed:meshHeading | pubmed-meshheading:15253693... | lld:pubmed |
| pubmed-article:15253693 | pubmed:meshHeading | pubmed-meshheading:15253693... | lld:pubmed |
| pubmed-article:15253693 | pubmed:meshHeading | pubmed-meshheading:15253693... | lld:pubmed |
| pubmed-article:15253693 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15253693 | pubmed:articleTitle | Ischemic acute renal failure: an inflammatory disease? | lld:pubmed |
| pubmed-article:15253693 | pubmed:affiliation | Medical Services, Brigham and Women's Hospital and Department of Medicine, Harvard Medical School, and Harvard-Massachusetts Institute of Technology, Division of Health Sciences and Technology, Charlestown, USA. joseph_bonventre@hms.harvard.edu | lld:pubmed |
| pubmed-article:15253693 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15253693 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15253693 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:15253693 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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