ArticleHerz2016
S100A4 and P53 in myocardial collagen fibers of hypertrophic cardiomyopathy : Expression and clinical significance.
Article in Herz, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 10 citations in OpenAlex.
- CD64 plays a key role in diabetic wound healing.Frontiers in immunology · 2024Article
- S100 proteins in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2023Review
- Cardiomyocyte Apoptosis Is Associated with Contractile Dysfunction in Stem Cell Model ofInternational journal of molecular sciences · 2023Article
- Cardiomyocyte apoptosis contributes to contractile dysfunction in stem cell model ofbioRxiv : the preprint server for biology · 2023Article
- The Roles of S100A4 and the EGF/EGFR Signaling Axis in Pulmonary Hypertension with Right Ventricular Hypertrophy.Biology · 2022Article
- Evaluation of the Effects ofEvidence-based complementary and alternative medicine : eCAM · 2020Article
- S100A4 as a Target of the E3-Ligase Asb2β and Its Effect on Engineered Heart Tissue.Frontiers in physiology · 2018Article
- Cardiac Troponin and Tropomyosin: Structural and Cellular Perspectives to Unveil the Hypertrophic Cardiomyopathy Phenotype.Frontiers in physiology · 2016Review
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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe purpose of this work is to investigate the expression of S100A4 and P53 and their correlation with myocardial collagen fibers in hypertrophic cardiomyopathy (HCM). PATIENTS AND
methodsMyocardial tissue obtained from 10 patients undergoing HCM surgery (HCM group) was compared to myocardial tissue obtained from 10 traffic accident deaths (healthy control group). Collagen volume fractions were visualized and compared using sirius red F3B(SR) staining. Immunohistochemistry S-P and in situ hybridization techniques were used to test the different expressions of S100A4, P53 proteins, and their mRNA. Imaging and statistical methods were used for quantitative analysis.
resultsThe collagen volume fraction in the HCM group was significantly higher than that in the control group. The integral optical density values of S100A4 and P53 in cardiomyocytes of the HCM group were also significantly higher than in the control group.
conclusionThe increased content of collagen fibers and overexpression of S100A4 and P53 may play an important role in myocardial fibrosis of HCM, and they can be used in future HCM research. Blockade of S100A4 may have therapeutic potential in HCM by attenuating cardiac fibrosis.
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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.