Linked Life Data

16932401

Source:http://linkedlifedata.com/resource/pubmed/id/16932401

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-8-25
pubmed:abstractText
Fibroblasts are one of the most important and episodically active cell types in the kidney. Under normal conditions, these cells provide a delicate collagenous matrix that partitions the interstitial spaces between nephrons, blood vessels and the renal capsule. Fibroblasts also remodel the interstitium as kidneys grow with age. This episodic activity of various fibroblast populations has a biological basis. Most fibroblasts are created locally through a process called epithelial-mesenchymal transition (EMT) and, once formed, they can proliferate in response to local mitogens. EMT is driven by an alteration in the balance of local cytokine concentrations that reverses the differentiation of selected epithelia along tubular nephrons. During persistent injury and inflammation, fibroblasts further increase their numbers and secrete excess interstitial collagens, and EMT is particularly aggressive in this setting. The mechanisms by which fibroblasts simultaneously destroy normal interstitial architecture and disable epithelial nephrons are more comprehensible today. Recent therapeutic clues for attenuating fibroblast formation during renal fibrogenesis also suggest an advantage in shifting local cytokine balance to favor mesenchymal-epithelial transition. This review examines these issues and identifies new targets for the treatment of one of the most difficult problems facing clinical nephrology.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1745-8323
pubmed:author
pubmed:issnType
Print
pubmed:volume
2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
101-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Mechanisms of disease: Fibroblasts--a new look at an old problem.
pubmed:affiliation
Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232-2358, USA. eric.neilson@vanderbilt.edu
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural