ArticleOncotarget2017
The optimization of cell therapy by combinational application with apicidin-treated mesenchymal stem cells after myocardial infarction.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 17 citations in OpenAlex.
- Histone Deacetylase Inhibitors as a Promising Treatment Against Myocardial Infarction: A Systematic Review.Journal of clinical medicine · 2024Review
- Mucosal TLR5 activation controls healthspan and longevity.Nature communications · 2024Article
- Multiparametric analysis of etoposide exposed mesenchymal stem cells and Fanconi anemia cells: implications in development of secondary myeloid malignancy.Clinical and experimental medicine · 2023Article
- PSME4 determines mesenchymal stem cell fate towards cardiac commitment through YAP1 degradation.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- PSME4 Degrades Acetylated YAP1 in the Nucleus of Mesenchymal Stem Cells.Pharmaceutics · 2022Article
- Consistent Long-Term Therapeutic Efficacy of Human Umbilical Cord Matrix-Derived Mesenchymal Stromal Cells After Myocardial Infarction Despite Individual Differences and Transient Engraftment.Frontiers in cell and developmental biology · 2021Article
- Research Progress on the Treatment of Premature Ovarian Failure Using Mesenchymal Stem Cells: A Literature Review.Frontiers in cell and developmental biology · 2021Review
- Role of YAP/TAZ in Cell Lineage Fate Determination and Related Signaling Pathways.Frontiers in cell and developmental biology · 2020Review
- Antiinflammatory activity of ANGPTL4 facilitates macrophage polarization to induce cardiac repair.JCI insight · 2019Article
- Adjuvant role of macrophages in stem cell-induced cardiac repair in rats.Experimental & molecular medicine · 2018Article
- Troponin through the looking-glass: emerging roles beyond regulation of striated muscle contraction.Oncotarget · 2018Review
- Functionally Improved Mesenchymal Stem Cells to Better Treat Myocardial Infarction.Stem cells international · 2018Review
- Functional Relevance of Macrophage-mediated Inflammation to Cardiac Regeneration.Chonnam medical journal · 2018Review
- Bone marrow CD34Stem cell research & therapy · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although mesenchymal stem cells (MSC) have been shown to be safe in preclinical studies of cardiovascular disease, multiple meta-analyses have debated whether functional improvement is significant or not. The cardiac differentiation from MSC is achievable using cardiogenic factors, however, the high cost and long culture period may limit the applications. Here, we developed a novel method to optimize the therapeutic outcome for myocardial infarction (MI). Treatment of MSC with apicidin, a histone deacetylase inhibitor, dramatically increased the expressions of cardiac markers such as GATA4, Nkx2.5, and cardiac troponin I (cTnI). In AC/MSC, stemness-related genes and yes-associated protein (YAP), a potent oncogene that drives cell proliferation, were significantly suppressed. Furthermore apicidin treatment or YAP knockdown downregulated miR-130a expression followed by induction of cardiac markers in MSC. In the comparison study, we found that both cardiac gene induction and angiogenesis were most prominent in the mixture of non-treated MSC and AC/MSC (Mix). Using mouse MI model, we show that application of Mix was strongly associated with cardiac differentiation of injected MSC and improved cardiac performance. Our results suggest that suppression of YAP/miR-130a shifts MSC cell fate toward cardiac lineage and identify apicidin as a potential pharmacological target for therapeutic development.
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.