ArticleStem cells (Dayton, Ohio)2019
CRISPR-Knockout Screen Identifies Dmap1 as a Regulator of Chemically Induced Reprogramming and Differentiation of Cardiac Progenitors.
Article in Stem cells (Dayton, Ohio), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Appraisal of CRISPR Technology as an Innovative Screening to Therapeutic Toolkit for Genetic Disorders.Molecular biotechnology · 2026Review
- Review
- In Vivo Targeted Reprogramming of Cardiac Fibroblasts for Heart Regeneration: Advances and Therapeutic Potential.Bioengineering (Basel, Switzerland) · 2025Review
- A chromatin-focused CRISPR screen identifies USP22 as a barrier to somatic cell reprogramming.Communications biology · 2025Article
- Direct Cardiac Reprogramming in the Age of Computational Biology.Journal of cardiovascular development and disease · 2024Review
- Genome-scale CRISPR-Cas9 screening in stem cells: theories, applications and challenges.Stem cell research & therapy · 2024Review
- Robust small molecule-aided cardiac reprogramming systems selective to cardiac fibroblasts.iScience · 2023Article
- Direct Reprogramming of Resident Non-Myocyte Cells and Its Potential for In Vivo Cardiac Regeneration.Cells · 2023Review
- CRISPR screening in cardiovascular research.Frontiers in cell and developmental biology · 2023Review
- Direct Cardiac Reprogramming: Current Status and Future Prospects.Advances in experimental medicine and biology · 2023Review
- Genome Editing and Cardiac Regeneration.Advances in experimental medicine and biology · 2023Article
- CRISPR activation of endogenous genes reprograms fibroblasts into cardiovascular progenitor cells for myocardial infarction therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Mapping regulators of cell fate determination: Approaches and challenges.APL bioengineering · 2020Review
- Cell Reprogramming With CRISPR/Cas9 Based Transcriptional Regulation Systems.Frontiers in bioengineering and biotechnology · 2020Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Direct in vivo reprogramming of cardiac fibroblasts into myocytes is an attractive therapeutic intervention in resolving myogenic deterioration. Current transgene-dependent approaches can restore cardiac function, but dependence on retroviral delivery and persistent retention of transgenic sequences are significant therapeutic hurdles. Chemical reprogramming has been established as a legitimate method to generate functional cell types, including those of the cardiac lineage. Here, we have extended this approach to generate progenitor cells that can differentiate into endothelial cells and cardiomyocytes using a single inhibitor protocol. Depletion of terminally differentiated cells and enrichment for proliferative cells result in a second expandable progenitor population that can robustly give rise to myofibroblasts and smooth muscle. Deployment of a genome-wide knockout screen with clustered regularly interspaced short palindromic repeats-guide RNA library to identify novel mediators that regulate the reprogramming revealed the involvement of DNA methyltransferase 1-associated protein 1 (Dmap1). Loss of Dmap1 reduced promoter methylation, increased the expression of Nkx2-5, and enhanced the retention of self-renewal, although further differentiation is inhibited because of the sustained expression of Cdh1. Our results hence establish Dmap1 as a modulator of cardiac reprogramming and myocytic induction. Stem Cells 2019;37:958-972.
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Registered trials
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