ReviewSeminars in cell & developmental biology2016
Can heart function lost to disease be regenerated by therapeutic targeting of cardiac scar tissue?
Review in Seminars in cell & developmental biology, 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
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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
8 citing papers in PubMed, 23 citations in OpenAlex.
- Transcriptional remodeling of cardiomyocytes and fibroblasts during post-myocardial infarction recovery.Scientific reports · 2026Article
- MBNL2 promotes aging-related cardiac fibrosis via inhibited SUMOylation of Krüppel-like factor4.iScience · 2024Article
- Identification of Natural Products as SENP2 Inhibitors for Targeted Therapy in Heart Failure.Frontiers in pharmacology · 2022Article
- Cardiac Connexin-43 Hemichannels and Pannexin1 Channels: Provocative Antiarrhythmic Targets.International journal of molecular sciences · 2020Review
- Alginate Formulations: Current Developments in the Race for Hydrogel-Based Cardiac Regeneration.Frontiers in bioengineering and biotechnology · 2020Review
- Modulation of retinoid signaling: therapeutic opportunities in organ fibrosis and repair.Pharmacology & therapeutics · 2020Review
- Injectable Hydrogels for Cardiac Tissue Engineering.Macromolecular bioscience · 2018Review
- Cardiac fibroblasts: from origin to injury.Current opinion in physiology · 2018Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Myocardial infarction results in scar tissue that cannot actively contribute to heart mechanical function and frequently causes lethal arrhythmias. The healing response after infarction involves inflammation, biochemical signaling, changes in cellular phenotype, activity, and organization, and alterations in electrical conduction due to variations in cell and tissue geometry and alterations in protein expression, organization, and function - particularly in membrane channels. The intensive research focus on regeneration of myocardial tissues has, as of yet, only met with modest success, with no near-term prospect of improving standard-of-care for patients with heart disease. An alternative concept for novel therapeutic approach is the rejuvenation of cardiac electrical and mechanical properties through the modification of scar tissue. Several peptide therapeutics, locally applied genetic therapies, or delivery of genetically modified cells have shown promise in improving the characteristics of the fibrous scar and post-myocardial infarction prognosis in experimental models. This review highlights several factors that contribute to arrhythmogenesis in scar formation and how these might be targeted to regenerate some of the electrical and mechanical function of the post-MI scar.
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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.