ReviewHistology and histopathology2017
The expression of Smad signaling pathway in myocardium and potential therapeutic effects.
Review in Histology and histopathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 10 citations in OpenAlex.
- A bibliometric analysis of myocardial fibrosis in diabetic cardiomyopathy: global trends and future directions.Journal of cardiothoracic surgery · 2026Article
- THR-123, a novel BMP-7 mimetic that activates Akt phosphorylation and inhibits cardiomyocyte apoptosis and inflammation, protects the heart from myocardial injury in a Rat model.Frontiers in cardiovascular medicine · 2026Article
- Salvianolic acid B ameliorates myocardial fibrosis in diabetic cardiomyopathy by deubiquitinating Smad7.Chinese medicine · 2023Article
- Activin A directly impairs human cardiomyocyte contractile function indicating a potential role in heart failure development.Frontiers in cardiovascular medicine · 2022Article
- RNAseq shows an all-pervasive day-night rhythm in the transcriptome of the pacemaker of the heart.Scientific reports · 2021Article
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 at 2 institutions in 2 countries.
Funding
Abstract
Myocardial infarction (MI) is a life-threatening disease. The expression of Smad proteins in the ischemic myocardium changes significantly following myocardial infarction, suggesting a close relationship between Smad proteins and heart remodeling. Moreover, it is known that the expression of Smads is regulated by transforming growth factor-β (TGF-β) and bone morphogenetic proteins (BMP). Based on these findings, regulating the expression of Smad proteins by targeting TGF-β and BMP in the ischemic myocardium may be considered to be a possible therapeutic strategy for the treatment of myocardial infarction.
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.