Tubulointerstitial renal disease. Export

@article{citeulike:5757058, abstract = {Tubulointerstitial damage, in progressive chronic renal disease of all types, arises because of a complex interplay between factors in the tubular lumen, tubular epithelial cells, peritubular capillaries, resident and infiltrating interstitial cells and extracellular matrix. Particularly in proteinuric renal disease, tubular epithelial cells play a central role in orchestrating these events. In response to mediators arising systemically, in the tubular lumen or from other renal cells, tubular epithelial cells undergo a complex series of structural and functional changes and produce a bewildering number of soluble and fixed mediators, which in turn lead to interstitial inflammation and fibrosis. Knowledge of these interactions has increased exponentially over the past decade, and has defined a number of new targets for treatment. Both expansion and consolidation of this knowledge is needed to determine which of these targets holds the most promise for future treatment.}, author = {Harris, D. C.}, citeulike-article-id = {5757058}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/11342791}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=11342791}, issn = {1062-4821}, journal = {Current opinion in nephrology and hypertension}, keywords = {emt, renal-fibrosis}, month = {May}, number = {3}, pages = {303--313}, posted-at = {2009-09-09 00:57:46}, priority = {2}, title = {Tubulointerstitial renal disease.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/11342791}, volume = {10}, year = {2001} }

TY - JOUR ID - citeulike:5757058 L3 - citeulike-article-id:5757058 N2 - Tubulointerstitial damage, in progressive chronic renal disease of all types, arises because of a complex interplay between factors in the tubular lumen, tubular epithelial cells, peritubular capillaries, resident and infiltrating interstitial cells and extracellular matrix. Particularly in proteinuric renal disease, tubular epithelial cells play a central role in orchestrating these events. In response to mediators arising systemically, in the tubular lumen or from other renal cells, tubular epithelial cells undergo a complex series of structural and functional changes and produce a bewildering number of soluble and fixed mediators, which in turn lead to interstitial inflammation and fibrosis. Knowledge of these interactions has increased exponentially over the past decade, and has defined a number of new targets for treatment. Both expansion and consolidation of this knowledge is needed to determine which of these targets holds the most promise for future treatment. IS - 3 JF - Current opinion in nephrology and hypertension SN - 1062-4821 EP - 313 TI - Tubulointerstitial renal disease. VL - 10 SP - 303 KW - emt KW - renal-fibrosis AU - Harris, DC PY - 2001/05// UR - http://view.ncbi.nlm.nih.gov/pubmed/11342791 ER -