ReviewPediatric nephrology (Berlin, Germany)2005
Can renal fibrosis be reversed?
Review in Pediatric nephrology (Berlin, Germany), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 52 citations in OpenAlex.
- Plasminogen Activation System and Fibroblasts: Impact on Tissue Remodeling, Disease, and Organ Homeostasis.Inflammation · 2026Review
- The Fate of Nephrons in Congenital Obstructive Nephropathy: Adult Recovery is Limited by Nephron Number Despite Early Release of Obstruction.The Journal of urology · 2015Article
- Immune system modulation of kidney regeneration--mechanisms and implications.Nature reviews. Nephrology · 2014Review
- Rotenone remarkably attenuates oxidative stress, inflammation, and fibrosis in chronic obstructive uropathy.Mediators of inflammation · 2014Article
- MicroRNA-328 inhibits renal tubular cell epithelial-to-mesenchymal transition by targeting the CD44 in pressure-induced renal fibrosis.PloS one · 2014Article
- Matrix metalloproteinases contribute to kidney fibrosis in chronic kidney diseases.World journal of nephrology · 2013Review
- Differential Ly-6C expression identifies the recruited macrophage phenotype, which orchestrates the regression of murine liver fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Liver fibrosis: a bidirectional model of fibrogenesis and resolution.QJM : monthly journal of the Association of Physicians · 2012Review
- Investigating mechanisms of chronic kidney disease in mouse models.Pediatric nephrology (Berlin, Germany) · 2012Review
- Mannose receptor 2 attenuates renal fibrosis.Journal of the American Society of Nephrology : JASN · 2012Article
- Telmisartan counteracts TGF-β1 induced epithelial-to-mesenchymal transition via PPAR-γ in human proximal tubule epithelial cells.International journal of clinical and experimental pathology · 2012Article
- Renal fibrosis.Korean journal of pediatrics · 2010Article
- Mechanisms of renal injury and progression of renal disease in congenital obstructive nephropathy.Pediatric nephrology (Berlin, Germany) · 2010Review
- Lentiviral-mediated RNA interference against TGF-beta receptor type II in renal epithelial and fibroblast cell populations in vitro demonstrates regulated renal fibrogenesis that is more efficient than a nonlentiviral vector.Journal of biomedicine & biotechnology · 2010Article
- Serine proteases, inhibitors and receptors in renal fibrosis.Thrombosis and haemostasis · 2009Review
- The renal cortical interstitium: morphological and functional aspects.Histochemistry and cell biology · 2008Review
- Urokinase and its receptors in chronic kidney disease.Frontiers in bioscience : a journal and virtual library · 2008Review
- Mineral metabolism and aging: the fibroblast growth factor 23 enigma.Current opinion in nephrology and hypertension · 2007Review
- Renal interstitial fibrosis and Angiotensin inhibition.Electrolyte & blood pressure : E & BP · 2006Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
New therapeutic approaches are needed to address the current epidemic of chronic kidney disease. Beyond delaying the inevitable onset of end-stage kidney disease the ultimate dream of clinical therapy is disease regression. Degradation of the interstitial matrix proteins is potentially feasible, especially before the interstitial "scar" becomes highly organized. Currently the specific matrix-degrading proteases that perform this function in vivo have not been clearly identified although several candidates have been suggested. Reversing renal fibrosis will also mandate removal of interstitial myofibroblasts that are the major source of the fibrosis-associated interstitial matrix proteins. However, the greater therapeutic challenge pertains to the current inability to regenerate intact functional nephrons in a site where they have been destroyed. In chronic tubulointerstitial damage that typifies all progressive kidney diseases, it is not interstitial matrix accumulation per se that leads to renal functional decline but rather its destructive effects on neighboring cells. In particular, loss of peritubular capillaries and tubules are the morphological features that underlie declining renal function. Recent advances in several basic scientific fields of investigation such as matrix biology, developmental biology, angiogenesis, and stem cell biology have identified new candidate therapeutic targets. A powerful new molecular tool-box is at our disposal that can be used to begin to translate recent discoveries into the clinical research arena with the goal of reversing renal fibrosis in a functionally meaningful way.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.