ReviewTranslational research : the journal of laboratory and clinical medicine2019
Cardiac fibrosis: potential therapeutic targets.
Review in Translational research : the journal of laboratory and clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 1 of them a synthesis that pooled it.
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
105 citing papers in PubMed, 1 synthesis or guideline pooled it, 214 citations in OpenAlex.
- Chitosan-Based Scaffolds for the Treatment of Myocardial Infarction: A Systematic Review.Molecules (Basel, Switzerland) · 2023Pooled it
- Chimeric antigen receptor T (CAR-T) cell therapy in non-oncological diseases.Signal transduction and targeted therapy · 2026Review
- TKT inhibition attenuates cardiac fibrosis in myocardial infarction through deactivating AKT signaling pathway.Journal of translational medicine · 2026Article
- Optimization of the in vitro Model of Cardiac Fibrosis.Brazilian journal of cardiovascular surgery · 2026Article
- Cardiac fibroblast heterogeneity in cardiac fibrosis implication for cell-type-specific treatment.Frontiers in physiology · 2026Review
- Therapeutic Targets for Myocardial Fibrosis: A Comprehensive Review of Current and Emerging Approaches.Cardiovascular & hematological disorders drug targets · 2026Review
- Role of HMGB1 in ischemia/reperfusion injury in a rat model of myocardial infarction.Scientific reports · 2025Article
- How Rapidly Does the FAPI PET Signal Reverse Following Therapy? Assessing the FAPI PET Signal in Hypertensive Cardiac Injury and Fibrosis in Mice.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025Article
- The role of progenitor cells and telocytes in the ameliorative effect of Coenzyme Q10 on isoproterenol-induced cardiotoxicity in rats.Histochemistry and cell biology · 2025Article
- Revolutionizing cardiac fibrosis treatment: the potential of personalized CAR T-cell therapy.Cardio-oncology (London, England) · 2025Review
- Cardiomyocyte regeneration after infarction: changes, opportunities and challenges.Molecular and cellular biochemistry · 2025Review
- The Role of the Extracellular Matrix in Inducing Cardiac Cell Regeneration and Differentiation.Cells · 2025Review
- Inhibiting the Histone Demethylase Kdm4a Restrains Cardiac Fibrosis After Myocardial Infarction by Promoting Autophagy in Premature Senescent Fibroblasts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- Dressed in Collagen: 2D and 3D Cardiac Fibrosis Models.International journal of molecular sciences · 2025Review
- Targeting the E Prostanoid Receptor EP4 Mitigates Cardiac Fibrosis Induced by β-Adrenergic Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Baricitinib represses the myocardial fibrosis via blocking JAK/STAT and TGF-β1 pathways in vivo and in vitro.BMC cardiovascular disorders · 2025Article
- Cardiac implications of chicken wooden breast myopathy.Frontiers in physiology · 2025Article
- Treating Cardiovascular Disorders with Personalized Medicine.Cardiovascular & hematological disorders drug targets · 2025Review
- Targeting Fibrosis: From Molecular Mechanisms to Advanced Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
45 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
4 authors at 1 institution in 1 country.
Funding
Abstract
Cardiovascular disease is a leading cause of mortality in the world and is exacerbated by the presence of cardiac fibrosis, defined by the accumulation of noncontractile extracellular matrix proteins. Cardiac fibrosis is directly linked to cardiac dysfunction and increased risk of arrhythmia. Despite its prevalence, there is a lack of efficacious therapies for inhibiting or reversing cardiac fibrosis, largely due to the complexity of the cell types and signaling pathways involved. Ongoing research has aimed to understand the mechanisms of cardiac fibrosis and develop new therapies for treating scar formation. Major approaches include preventing the formation of scar tissue and replacing fibrous tissue with functional cardiomyocytes. While targeting the renin-angiotensin-aldosterone system is currently used as the standard line of therapy for heart failure, there has been increased interest in inhibiting the transforming growth factor-β signaling pathway due its established role in cardiac fibrosis. Significant advances in cell transplantation therapy and biomaterials engineering have also demonstrated potential in regenerating the myocardium. Novel techniques, such as cellular direct reprogramming, and molecular targets, such as noncoding RNAs and epigenetic modifiers, are uncovering novel therapeutic options targeting fibrosis. This review provides an overview of current approaches and discuss future directions for treating cardiac fibrosis.
Indexed as
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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.