| Mediators of inflammation in acute kidney injury. | |
| | |
MedLine Citation:
|
PMID: 20182538 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
Acute kidney injury (AKI) remains to be an independent risk factor for mortality and morbidity. Inflammation is now believed to play a major role in the pathophysiology of AKI. It is hypothesized that in ischemia, sepsis and nephrotoxic models that the initial insult results in morphological and/or functional changes in vascular endothelial cells and/or in tubular epithelium. Then, leukocytes including neutrophils, macrophages, natural killer cells, and lymphocytes infiltrate into the injured kidneys. The injury induces the generation of inflammatory mediators like cytokines and chemokines by tubular and endothelial cells which contribute to the recruiting of leukocytes into the kidneys. Thus, inflammation has an important role in the initiation and extension phases of AKI. This review will focus on the mediators of inflammation contributing to the pathogenesis of AKI. |
| | |
Authors:
|
Ali Akcay; Quocan Nguyen; Charles L Edelstein |
Related Documents
:
|
10644878 - 15-lipoxygenase in glomerular inflammation. 8387828 - Endothelium-derived relaxing factor, nitric oxide: effects on and production by mesangi... 19034328 - Experimental induction of salt-sensitive hypertension is associated with lymphocyte pro... 1600138 - Renal growth responses to acute and chronic injury: routes to therapeutic intervention. 10733268 - Apoptosis in primary cutaneous amyloidosis. 15494978 - Tissue plasminogen activator and glial function. |
Publication Detail:
|
Type: Journal Article; Research Support, N.I.H., Extramural; Review Date: 2010-02-21 |
Journal Detail:
|
Title: Mediators of inflammation Volume: 2009 ISSN: 1466-1861 ISO Abbreviation: Mediators Inflamm. Publication Date: 2009 |
Date Detail:
|
Created Date: 2010-02-25 Completed Date: 2010-05-04 Revised Date: 2010-09-30 |
Medline Journal Info:
|
Nlm Unique ID: 9209001 Medline TA: Mediators Inflamm Country: United States |
Other Details:
|
Languages: eng Pagination: 137072 Citation Subset: IM |
Affiliation:
|
Division of Renal Diseases and Hypertension, University of Colorado Denver, Aurora, CO 80262, USA. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Cell Adhesion Molecules
/
metabolism Chemokines / immunology Complement System Proteins / immunology Cytokines / immunology Endoplasmic Reticulum / metabolism Endothelial Cells / cytology, metabolism Humans Inflammation / metabolism* Inflammation Mediators / metabolism* Kidney Failure, Acute / mortality, pathology, physiopathology* Kidney Tubules / metabolism, pathology Stress, Physiological Toll-Like Receptors / immunology |
| Grant Support | |
ID/Acronym/Agency:
|
R01-DK-056851/DK/NIDDK NIH HHS; R01-DK-074835/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
|
0/Cell Adhesion Molecules; 0/Chemokines; 0/Cytokines; 0/Inflammation Mediators; 0/Toll-Like Receptors; 9007-36-7/Complement System Proteins |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Optical spectroscopy for noninvasive monitoring of stem cell differentiation.
Next Document: Evasion of apoptosis as a cellular stress response in cancer.