ArticleBulletin of experimental biology and medicine2025
Search for Molecular Markers of Myocardial Injury in a Mouse Model of Obstructive Nephropathy Using Nestin Promoter-Driven GFP Expression.
Article in Bulletin of experimental biology and medicine, 2025. 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression of cardiac dysfunction markers and the number of nestin-positive cells in the myocardium were analyzed in a mouse model of obstructive nephropathy using animals expressing GFP under the nestin promoter. Unilateral ureteral obstruction (UUO) led to an increase in the number of nestin-positive cells in cardiac tissue, accompanied by elevated expression of B-type natriuretic peptide, which positively correlated with GFP levels. A trend toward reduced expression of β-myosin heavy chain and the gap junction protein connexin-43 was observed, whereas the expression of the progenitor cell marker WT1 remained unchanged under UUO conditions. These findings indicate the development of cardiac dysfunction in this model is secondary to primary renal injury and highlight a concomitant expansion of nestin-positive cells within the myocardium.
Indexed as
Identifiers
41661429What Socratic 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 Socratic graph.