ArticleNature communications2015
High-efficiency reprogramming of fibroblasts into cardiomyocytes requires suppression of pro-fibrotic signalling.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 148 papers, 2 of them syntheses 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
148 citing papers in PubMed, 2 syntheses or guidelines pooled it, 229 citations in OpenAlex.
- A Bibliometric and Visualized Analysis of Cardiac Regeneration Over a 20-Year Period.Frontiers in cardiovascular medicine · 2021Pooled it
- 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
- SNAI2/SLUG: a key regulator of endothelial-to-mesenchymal transition and vascular remodeling in cardiovascular diseases.Journal of cardiothoracic surgery · 2026Review
- The cardiac 4D nucleome: nuclear and chromatin dynamics across development, disease and ageing.Nature reviews. Cardiology · 2026Review
- Electrical coupling between transplanted cardiomyocytes and host myocardium to prevent arrhythmia.Disease models & mechanisms · 2026Review
- Simulation-guided chemical direct reprogramming informed by temporal cellular conversion processes at the single-cell level.Communications chemistry · 2026Article
- Atorvastatin Attenuates Human Cardiac Fibroblast Activation, with Associated Changes in GATA4/MEF2C and Selected Fibrosis-Related microRNAs.International journal of molecular sciences · 2026Article
- HDAC11 Regulates RNA Splicing via De-Fatty Acylation of SF3B2.bioRxiv : the preprint server for biology · 2026Article
- Heart Regeneration for Clinical Application.Internal medicine (Tokyo, Japan) · 2026Review
- A tripartite therapeutic agent reprograms the myocardial infarction microenvironment.Materials today. Bio · 2025Article
- Advances in fibroblast-based cardiac reprogramming in the treatment of heart disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- Vaxtherapy, a Multiphase Therapeutic Protocol Approach for Longvax, the COVID-19 Vaccine-Induced Disease: Spike Persistence as the Core Culprit and Its Downstream Effects.Diseases (Basel, Switzerland) · 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
- Decoding the epigenetic and transcriptional basis of direct cardiac reprogramming.Stem cells (Dayton, Ohio) · 2025Review
- Direct fibroblast reprogramming: an emerging strategy for treating organic fibrosis.Journal of translational medicine · 2025Review
- Macrophages suppress cardiac reprogramming of fibroblasts in vivo via IFN-mediated intercellular self-stimulating circuit.Protein & cell · 2024Article
- Control of cell fate upon transcription factor-driven cardiac reprogramming.Current opinion in genetics & development · 2024Review
- In situ reprogramming of cardiac fibroblasts into cardiomyocytes in mouse heart with chemicals.Acta pharmacologica Sinica · 2024Article
88 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
12 authors at 2 institutions in 1 country.
Funding
Abstract
Direct reprogramming of fibroblasts into cardiomyocytes by forced expression of cardiomyogenic factors, GMT (GATA4, Mef2C, Tbx5) or GHMT (GATA4, Hand2, Mef2C, Tbx5), has recently been demonstrated, suggesting a novel therapeutic strategy for cardiac repair. However, current approaches are inefficient. Here we demonstrate that pro-fibrotic signalling potently antagonizes cardiac reprogramming. Remarkably, inhibition of pro-fibrotic signalling using small molecules that target the transforming growth factor-β or Rho-associated kinase pathways converts embryonic fibroblasts into functional cardiomyocyte-like cells, with the efficiency up to 60%. Conversely, overactivation of these pro-fibrotic signalling networks attenuates cardiac reprogramming. Furthermore, inhibition of pro-fibrotic signalling dramatically enhances the kinetics of cardiac reprogramming, with spontaneously contracting cardiomyocytes emerging in less than 2 weeks, as opposed to 4 weeks with GHMT alone. These findings provide new insights into the molecular mechanisms underlying cardiac conversion of fibroblasts and would enhance efforts to generate cardiomyocytes for clinical applications.
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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.