ArticleStem cell reports2017
Notch Inhibition Enhances Cardiac Reprogramming by Increasing MEF2C Transcriptional Activity.
Article in Stem cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.
What it found
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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
79 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.
- Cardiac Regeneration: New Insights Into the Frontier of Ischemic Heart Failure Therapy.Frontiers in bioengineering and biotechnology · 2020Pooled it
- Integrating delivery systems and microenvironmental cues to accelerate clinical translation of cardiac reprogramming.Materials today. Bio · 2026Review
- Macrophage Mistargeting During Direct Cardiac Reprogramming: Cardiac-Associated Responses, Polarization, and Cell Death.Biomedicines · 2026Article
- Running exercise alleviates chronic heart failure by promoting cardiomyocyte autophagic flux through the NEAT1-QKI affecting Beclin1/LC3B mRNA stability.Biology direct · 2026Article
- Biologics for cardiovascular diseases: from bench to bedside.Signal transduction and targeted therapy · 2026Review
- Administration of a novel reprogramming formula improves cardiac function and decreases cardiac fibrosis in a myocardial infarction model.JTCVS open · 2025Article
- A novel Notch and WNT signaling mechanism contribute to paediatric DCM: a pathway to new therapeutics.bioRxiv : the preprint server for biology · 2025Article
- Cell Reprogramming, Transdifferentiation, and Dedifferentiation Approaches for Heart Repair.International journal of molecular sciences · 2025Review
- Cell reprogramming: methods, mechanisms and applications.Cell regeneration (London, England) · 2025Review
- Research Advances in Myocardial Infarction Repair and Cardiac Regenerative Medicine via the Notch Signaling Pathway.Reviews in cardiovascular medicine · 2025Review
- Next-generation direct reprogramming.Frontiers in cell and developmental biology · 2024Review
- Robust small molecule-aided cardiac reprogramming systems selective to cardiac fibroblasts.iScience · 2023Article
- Recent advances and future prospects in direct cardiac reprogramming.Nature cardiovascular research · 2023Review
- Cellular reprogramming of fibroblasts in heart regeneration.Journal of molecular and cellular cardiology · 2023Review
- Regeneration of the heart: from molecular mechanisms to clinical therapeutics.Military Medical Research · 2023Review
- Direct Reprogramming of Resident Non-Myocyte Cells and Its Potential for In Vivo Cardiac Regeneration.Cells · 2023Review
- Regulation of Cell Plasticity by Bromodomain and Extraterminal Domain (BET) Proteins: A New Perspective in Glioblastoma Therapy.International journal of molecular sciences · 2023Review
- Generation of dorsoventral human spinal cord organoids via functionalizing composite scaffold for drug testing.iScience · 2023Article
- Transcriptional and functional consequences of alterations to MEF2C and its topological organization in neuronal models.American journal of human genetics · 2022Article
- The Role of the Notch Signaling Pathway in Recovery of Cardiac Function after Myocardial Infarction.International journal of molecular sciences · 2022Review
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Conversion of fibroblasts into functional cardiomyocytes represents a potential means of restoring cardiac function after myocardial infarction, but so far this process remains inefficient and little is known about its molecular mechanisms. Here we show that DAPT, a classical Notch inhibitor, enhances the conversion of mouse fibroblasts into induced cardiac-like myocytes by the transcription factors GATA4, HAND2, MEF2C, and TBX5. DAPT cooperates with AKT kinase to further augment this process, resulting in up to 70% conversion efficiency. Moreover, DAPT promotes the acquisition of specific cardiomyocyte features, substantially increasing calcium flux, sarcomere structure, and the number of spontaneously beating cells. Transcriptome analysis shows that DAPT induces genetic programs related to muscle development, differentiation, and excitation-contraction coupling. Mechanistically, DAPT increases binding of the transcription factor MEF2C to the promoter regions of cardiac structural genes. These findings provide mechanistic insights into the reprogramming process and may have important implications for cardiac regeneration therapies.
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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.