ReviewThe Journal of clinical investigation2022
Therapeutic targets for cardiac fibrosis: from old school to next-gen.
Review in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 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
80 citing papers in PubMed, 160 citations in OpenAlex.
- New approach methodologies: drug screening platform to identify antifibrotic compounds.Nature protocols · 2026Review
- A practical toolbox for modelling fibrosis in vitro.Nature biomedical engineering · 2026Review
- Heart-on-a-chip and vasculature-on-a-chip platforms as models of cardiovascular disease.Nature reviews. Cardiology · 2026Review
- Urea cycle fumarate limits fibrosis post-myocardial infarction by reducing fibroblast mitochondrial adenosine triphosphate production.Cardiovascular research · 2026Article
- Fibroblasts: a diverse population of cells balancing homeostasis, wound healing, regeneration, inflammation, fibrosis, and cancer across organs.JCI insight · 2026Review
- Accelerated Turnover of Collagens and Other Extracellular Matrix Proteins Upon Chronic Beta-Adrenergic Stimulation.JACC. Basic to translational science · 2026Article
- Myocardial Fibrosis in Cardiovascular Disease: An Integrative Biomarker-Imaging Framework Linking Molecular Mechanisms to Structural Phenotypes.Journal of clinical medicine · 2026Review
- ML216 Alleviates Age-Related Cardiac Fibrosis by Suppressing TGF-β1 Signaling Pathway.International journal of molecular sciences · 2026Article
- Dimethyl Fumarate Reverses β-Adrenoceptor-Mediated Myocardial Fibrosis in Mice by Inhibiting Yes-Associated Protein-Regulated Expression of Intermediate-Conductance CaJournal of the American Heart Association · 2026Article
- VAP1 promotes cardiac fibrosis by enabling PDGFR signaling in myofibroblasts.Experimental & molecular medicine · 2026Article
- Injectable alginate composite hydrogel with spatiotemporal codelivery of pro-angiogenic and anti-fibrotic agents for synergistic myocardial repair.Materials today. Bio · 2026Article
- Decoding organ fibrosis: mechanistic insights and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- SLC31A1 exon 1 methylation reduces intracellular copper ion and promotes diabetic cardiac fibrosis.Cardiovascular diabetology · 2026Article
- Design of RGD-functionalized GSH-responsive pegylated polymeric protacs for selective BRD4 degradation and EndMT-driven cardiac fibrosis inhibition.Journal of nanobiotechnology · 2026Article
- Therapeutic Targets for Myocardial Fibrosis: A Comprehensive Review of Current and Emerging Approaches.Cardiovascular & hematological disorders drug targets · 2026Review
- The Role of Thrombospondin-2 in Myocardial Fibrosis.Drug design, development and therapy · 2026Review
- The interaction between sarcoplasmic reticulum and mitochondria: a novel mechanism for cardiac arrhythmia.Frontiers in physiology · 2026Review
- PMAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Deep-DPC: Deep learning-assisted label-free temporal imaging discovery of anti-fibrotic compounds by controlling cell morphology.Journal of advanced research · 2025Article
- Identification of epigenetic regulators of fibrotic transformation in cardiac fibroblasts through bulk and single-cell CRISPR screens.Nature communications · 2025Article
20 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 diseases remain the leading cause of death worldwide, with pathological fibrotic remodeling mediated by activated cardiac myofibroblasts representing a unifying theme across etiologies. Despite the profound contributions of myocardial fibrosis to cardiac dysfunction and heart failure, there currently exist limited clinical interventions that effectively target the cardiac fibroblast and its role in fibrotic tissue deposition. Exploration of novel strategies designed to mitigate or reverse myofibroblast activation and cardiac fibrosis will likely yield powerful therapeutic approaches for the treatment of multiple diseases of the heart, including heart failure with preserved or reduced ejection fraction, acute coronary syndrome, and cardiovascular disease linked to type 2 diabetes. In this Review, we provide an overview of classical regulators of cardiac fibrosis and highlight emerging, next-generation epigenetic regulatory targets that have the potential to revolutionize treatment of the expanding cardiovascular disease patient population.
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What Socratic 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 Socratic graph.