ReviewBiomaterials research2016
Antifibrotic therapies to control cardiac fibrosis.
Review in Biomaterials research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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
73 citing papers in PubMed.
- Leptin Activates Brain-BAT-Heart Crosstalk to Promote Cardiac Protection.Circulation research · 2026Article
- Comparative Effects of Repeated Intravenous Infusions of Progenitor Cells in a Rat Model of Chronic Ischemic Cardiomyopathy.Stem cell reviews and reports · 2026Article
- Therapeutic Targets for Myocardial Fibrosis: A Comprehensive Review of Current and Emerging Approaches.Cardiovascular & hematological disorders drug targets · 2026Review
- Engineered T cell therapy for the treatment of cardiac fibrosis during chronic phase of myocarditis.Theranostics · 2026Article
- Revolutionizing cardiac fibrosis treatment: the potential of personalized CAR T-cell therapy.Cardio-oncology (London, England) · 2025Review
- Zhilong Huoxue Tongyu capsule inhibits hypertensive myocardial fibrosis via balancing TGF-β1/Smad3/Erbb4-IR/miR-29b pathway.Scientific reports · 2025Article
- Cardiac Fibroblasts: Helping or Hurting.Genes · 2025Review
- Nanomedicine for Diagnosis and Treatment of Cardiac Fibrosis.International journal of nanomedicine · 2025Review
- Bibliometrics of trends in global research on the roles of stem cells in myocardial fibrosis therapy.World journal of stem cells · 2024Article
- Cardiac tissue-resident vesicles differentially modulate anti-fibrotic phenotype by age and sex through synergistic miRNA effects.Biomaterials · 2024Article
- Limiting extracellular matrix expansion in diet-induced obese mice reduces cardiac insulin resistance and prevents myocardial remodelling.Molecular metabolism · 2024Article
- Relation between cardiac magnetic resonance-assessed interstitial fibrosis and diastolic dysfunction in heart failure due to dilated cardiomyopathy.International journal of cardiology. Heart & vasculature · 2024Article
- Tongxinluo Activates PI3K/AKT Signaling Pathway to Inhibit Endothelial Mesenchymal Transition and Attenuate Myocardial Fibrosis after Ischemia-Reperfusion in Mice.Chinese journal of integrative medicine · 2024Article
- Modified mRNA-MediatedInternational journal of molecular sciences · 2024Article
- Logic-based mechanistic machine learning on high-content images reveals how drugs differentially regulate cardiac fibroblasts.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Review
- Fibroblast-derived extracellular vesicles as trackable efficient transporters of an experimental nanodrug with fibrotic heart and lung targeting.Theranostics · 2024Article
- Logic-based mechanistic machine learning on high-content images reveals how drugs differentially regulate cardiac fibroblasts.bioRxiv : the preprint server for biology · 2023Article
- Extracellular vesicles: emerging roles, biomarkers and therapeutic strategies in fibrotic diseases.Journal of nanobiotechnology · 2023Review
- Hydrogel-Inducing Graphene-Oxide-Derived Core-Shell Fiber Composite for Antibacterial Wound Dressing.International journal of molecular sciences · 2023Article
13 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
2 authors.
Funding
Abstract
Cardiac fibrosis occurs naturally after myocardial infarction. While the initially formed fibrotic tissue prevents the infarcted heart tissue from rupture, the progression of cardiac fibrosis continuously expands the size of fibrotic tissue and causes cardiac function decrease. Cardiac fibrosis eventually evolves the infarcted hearts into heart failure. Inhibiting cardiac fibrosis from progressing is critical to prevent heart failure. However, there is no efficient therapeutic approach currently available. Myofibroblasts are primarily responsible for cardiac fibrosis. They are formed by cardiac fibroblast differentiation, fibrocyte differentiation, epithelial to mesenchymal transdifferentiation, and endothelial to mesenchymal transition, driven by cytokines such as transforming growth factor beta (TGF-β), angiotensin II and platelet-derived growth factor (PDGF). The approaches that inhibit myofibroblast formation have been demonstrated to prevent cardiac fibrosis, including systemic delivery of antifibrotic drugs, localized delivery of biomaterials, localized delivery of biomaterials and antifibrotic drugs, and localized delivery of cells using biomaterials. This review addresses current progresses in cardiac fibrosis therapies.
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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.