Molecular basis of renal fibrosis
By A. Eddy. Pediatric nephrology (Berlin, West), 2000
654 citations recorded by the source corpus.
Subfields: Molecular Biology, Nephrology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/bfdd1471a4fccd59e809a0132cdb989d1ff5e495
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In Nephrology
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Citations in the corpus
- Ureteral obstruction as a model of renal interstitial fibrosis and obstructive nephropathy. (2009, background): “On one hand, renal interstitial matrix accumulation is regarded as a primary cause of peritubular capillary obliteration, tubular atrophy, and progressive renal insufficiency.(27) The alternate view is that renal inflammation leads to glomerular and tubular damage of some nephrons, which in turn lea”
- Epithelial to mesenchymal transition in renal fibrogenesis: pathologic significance, molecular mechanism, and therapeutic intervention. (2004, background): “Over the years, the primary focus of tubulointerstitial fibrosis studies is on interstitial fibroblasts and infiltrated mononuclear cells for the obvious reasons (1,18,41).”
- The extracellular matrix: an active or passive player in fibrosis? (2011, background): “It is often considered to be an aberrant form of wound healing in which there is progression rather than resolution of scarring, resulting in excessive accumulation of ECM, thus causing disruption of normal tissue architecture and function (15).”
- Cellular and molecular mechanisms of renal fibrosis (2011, background): “On the basis of the sequence of these destructive events, the pathogenesis of renal fibrosis can be artificially divided into four overlapping phases: priming, activation, execution and progression”
- PAI-1 in Tissue Fibrosis (2012, background): “Numerous studies established a strong link between elevated levels of PAI-1 with glomerulosclerosis and kidney fibrosis (Eddy, 2000; Ma and Fogo, 2009).”
- Cellular and molecular mechanisms in kidney fibrosis. (2014, neutral): “The healthy kidney is a site of high collagen turnover (98).”