ReviewWorld journal of urology1995
Peptide growth factors in normal and hypertrophied bladder.
Review in World journal of urology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 27 citations in OpenAlex.
- Characterization of global and region-specific transcriptomic alterations in the bladder following acute partial bladder outlet obstruction in female mini-swine.Physiological reports · 2026Article
- Overactive bladder phenotype induced by chronic activation of hypothalamic neuroendocrine stress pathways in rats with no extrinsic behavioral stress applied.Scientific reports · 2025Article
- Article
- Role for pAKT in rat urinary bladder with cyclophosphamide (CYP)-induced cystitis.American journal of physiology. Renal physiology · 2011Article
- Endogenous nerve growth factor regulates collagen expression and bladder hypertrophy through Akt and MAPK pathways during cystitis.The Journal of biological chemistry · 2010Article
- Up-regulation of calcitonin gene-related peptide and receptor tyrosine kinase TrkB in rat bladder afferent neurons following TNBS colitis.Experimental neurology · 2007Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The bladder is a dynamic organ that responds to the stress of outlet obstruction by rapidly increasing in mass and cellular content to compensate for increased urethral resistance. If the outlet obstruction is released prior to decompensation, the hypertrophied bladder will shrink, returning to normal size and cellularity. However, with chronic obstruction the bladder will continue to increase in mass, developing drastic alterations in the amount and composition of the extracellular matrix and, ultimately, losing the ability to function. The extensive tissue remodeling associated with each of these changes requires different bladder components to undergo cellular proliferation, cellular hypertrophy, and even programmed cell death (apoptosis). Each of these cellular processes is known to be regulated by various peptides that are referred to as growth factors. Herein we provide an overview of the growth factors that are known to influence the bladder in addition to a variety of experimental animal studies that putatively identify a role of four particular growth factors [basic fibroblast growth factor (bFGF), transforming growth factor-beta (TGF-beta), nerve growth factor (NGF), and epidermal growth factor (EGF)] in the obstructive bladder response.
Indexed as
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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.