ReviewJournal of veterinary internal medicine2026
Transforming growth factor-β in kidney disease in dogs and cats: a review of the evidence of its role in renal fibrosis.
Review in Journal of veterinary internal medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A growing body of literature implicates the transforming growth factor (TGF)-β pathway in the progression of chronic kidney disease (CKD) in dogs and cats by promoting renal fibrosis. In rodents and humans, TGF-β is a key player in development of glomerulosclerosis and renal interstitial fibrosis. The pathway is also immunomodulatory, underscoring the complexity of its downstream effects. Recently, evidence for the role of TGF-β in small animal CKD has been presented using multiple methodologies, including serum and urinary biomarkers, as well as gene and protein expression in renal tissue and primary renal cell cultures. The aim of this review is to integrate these data and highlight consistencies and discrepancies in the literature. Some of the most convincing data supporting the role of the TGF-β pathway includes biomarker levels and pathway analysis of transcriptional profiles in spontaneous CKD in cats and in the X-linked Alport model in dogs. Demonstration of the presence of TGF-β protein is challenging due to lack of commercially available immunohistochemistry (IHC) antibodies that are sensitive and specific for active variants and isoforms TGF-β in dogs and cats. Cross-reactivity of IHC antibodies with latent TGF-β isoforms (complexed with extracellular matrix proteins) complicates the interpretation of IHC labeling. The mechanisms by which TGF-β activates fibroblasts and injures glomeruli in small animals is an area for future research. Although the relationship between TGF-β and glomerulosclerosis is mostly theoretical based on extrapolation from humans and rodents, substantial evidence strongly supports a role for TGF-β in renal interstitial scarring of small animals.
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.