ReviewNature reviews. Cardiology2013
Myofibroblast-mediated mechanisms of pathological remodelling of the heart.
Review in Nature reviews. Cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 355 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
355 citing papers in PubMed, 657 citations in OpenAlex.
- Trial
- Atrial cardiomyopathy: from knowledge gaps to clinical impact : The role of the EmbRACE Network.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2026Article
- Human Epididymis Protein 4 in Cardiovascular Disease: A Fibrosis-Driven Mediator of Tissue Remodeling and Inter-Organ Communication.Circulation reports · 2026Review
- Lactylation at the metabolic-epigenetic interface in cardiovascular diseases: context-dependent mechanisms and translational roadmap.Journal of advanced research · 2026Review
- Roles of inflammation and metabolic dysfunction in cardiovascular diseases: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Arrhythmic Mitral Valve Prolapse as a Regional Stretch-Induced Cardiomyopathy with Fibro-Inflammatory Signature: A Conceptual Review.Journal of cardiovascular development and disease · 2026Review
- Mitochondrial electron transport chain is essential for acute inflammatory stress responses in mouse fibroblasts.Scientific reports · 2026Article
- Extracellular Vesicles in Cardiac Cell Crosstalk: from Intercellular Communication to Clinical Translation.Cardiovascular drugs and therapy · 2026Review
- Outcomes by cardiovascular magnetic resonance in patients with clinically suspected myocardial inflammation.The international journal of cardiovascular imaging · 2026Article
- Protective Effects of 5-MTP in a Rat Model of Diabetic Cardiomyopathy Through Anti-Inflammatory, Anti-Apoptotic, and Antifibrotic Mechanisms.Life (Basel, Switzerland) · 2026Article
- Clinical implications of left anterior fascicular block for cardiac remodeling in hypertensive patients.Journal of echocardiography · 2026Article
- Recovery From Heart Failure: Microvascular Mechanisms.Circulation · 2026Article
- Changes in myocardial elasticity derived from in-vivo cardiac MRI in a swine model of ischemic heart failure.Scientific reports · 2026Article
- Cardiac fibroblasts in myocardial injury and heart failure.European heart journal · 2026Review
- Subclinical Inflammation in Ischemic Heart Disease and Its Role in the Transition to Heart Failure.Life (Basel, Switzerland) · 2026Review
- Zinc finger BED-type containing 6 (ZBED6) ameliorates cardiac fibrosis by inhibiting Piezo1 transcription and YAP nuclear translocation.Acta pharmacologica Sinica · 2026Article
- GPT2-mediated Glutamate to α-Ketoglutaric Acid Conversion in Cardiac Fibroblast Promotes Fibrosis.JACC. Basic to translational science · 2026Article
- FGF23 Controls Myocardial Fibrosis Progression via Promoting Cardiac Fibroblast Proliferation and Activation in Mice.Biology · 2026Article
- Endothelial-to-Mesenchymal Transition in Post-Myocardial Infarction Fibrosis: A Maladaptive but Targetable Pathway.EJIFCC · 2026Review
- Mechanical unloading coupled with coronary reperfusion stimulates cardiomyocyte proliferation and prevents unloading-induced fibrosis after myocardial infarction.Basic research in cardiology · 2026Article
295 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
5 authors at 1 institution in 1 country.
Funding
Abstract
The syncytium of cardiomyocytes in the heart is tethered within a matrix composed principally of type I fibrillar collagen. The matrix has diverse mechanical functions that ensure the optimal contractile efficiency of this muscular pump. In the diseased heart, cardiomyocytes are lost to necrotic cell death, and phenotypically transformed fibroblast-like cells-termed 'myofibroblasts'-are activated to initiate a 'reparative' fibrosis. The structural integrity of the myocardium is preserved by this scar tissue, although at the expense of its remodelled architecture, which has increased tissue stiffness and propensity to arrhythmias. A persisting population of activated myofibroblasts turns this fibrous tissue into a living 'secretome' that generates angiotensin II and its type 1 receptor, and fibrogenic growth factors (such as transforming growth factor-β), all of which collectively act as a signal-transducer-effector signalling pathway to type I collagen synthesis and, therefore, fibrosis. Persistent myofibroblasts, and the resultant fibrous tissue they produce, cause progressive adverse myocardial remodelling, a pathological hallmark of the failing heart irrespective of its etiologic origin. Herein, we review relevant cellular, subcellular, and molecular mechanisms integral to cardiac fibrosis and consequent remodelling of atria and ventricles with a heterogeneity in cardiomyocyte size. Signalling pathways that antagonize collagen fibrillogenesis provide novel strategies for cardioprotection.
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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.