ReviewCellular and molecular life sciences : CMLS2014
The pathogenesis of cardiac fibrosis.
Review in Cellular and molecular life sciences : CMLS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 899 papers, 3 of them syntheses 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
899 citing papers in PubMed, 3 syntheses or guidelines pooled it, 1,539 citations in OpenAlex.
- Anti-fibrosis effect of astragaloside IV in animal models of cardiovascular diseases and its mechanisms: a systematic review.Pharmaceutical biology · 2025Pooled it
- T1 mapping and major cardiovascular events in non-ischaemic dilated cardiomyopathy: a systematic review and meta-analysis.ESC heart failure · 2025Pooled it
- The influence of HIV infection on myocardial fibrosis diagnosed by cardiac magnetic resonance imaging in adults: a systematic review and meta-analysis of observation studies.Frontiers in cardiovascular medicine · 2025Pooled it
- Breaking the cycle of fibrosis: Ferroptosis as a therapeutic target (Review).International journal of molecular medicine · 2026Review
- Targeting receptor tyrosine kinases: from molecular mechanisms to clinical therapeutics.Signal transduction and targeted therapy · 2026Review
- Rigosertib Reverses Hypertrophic Cardiomyopathy in Noonan Syndrome.Circulation · 2026Article
- Chimeric antigen receptor T (CAR-T) cell therapy in non-oncological diseases.Signal transduction and targeted therapy · 2026Review
- HarnessingFood science & nutrition · 2026Review
- Macrophage Mistargeting During Direct Cardiac Reprogramming: Cardiac-Associated Responses, Polarization, and Cell Death.Biomedicines · 2026Article
- Collagen Prolyl 4-Hydroxylase: An Emerging Key Player in Cardiac Fibrosis.Journal of cardiovascular translational research · 2026Review
- Ellagic acid attenuates myocardial fibrosis by suppressing Bmi1-mediated inhibition of the p53/p21 pathway in cardiac fibroblasts.Molecular and cellular biochemistry · 2026Article
- Increased NETosis in Patients With Heart Failure Is Associated With Macrophage Activation Towards a Proinflammatory Phenotype.Journal of cellular and molecular medicine · 2026Article
- Pharmacological Inhibition of Small Extracellular Vesicle Secretion by ALK5i SD-208 via Lysosomal Rerouting of CD63+ Compartments.Journal of extracellular vesicles · 2026Article
- Cardiac magnetic resonance imaging reveals myocardial fibrosis and systolic dysfunction in mitochondrial trifunctional protein-deficient mice.Disease models & mechanisms · 2026Article
- Role of ATOH8 in Mitigating Cardiac Fibrosis in Heart Failure via Inhibition of the Transcriptional Repression of Smad7 by RUNX2.Biomolecules & therapeutics · 2026Article
- Nicotinamide Mononucleotide Ameliorates Myocardial Fibrosis in Diabetic Mice Possibly by Modulating SIRT3 to Deacetylate GSK3β and Thereby Reducing the Phosphorylation of Smad3.Journal of cardiovascular translational research · 2026Article
- Lipofuscin: Wear Pigment or Alarm Signal for Cardiac AlloGraft Vasculopathy?Diagnostics (Basel, Switzerland) · 2026Article
- Pathophysiology and Perioperative Considerations for Heart Failure Patients.Life (Basel, Switzerland) · 2026Review
- Ubiquitin-Related Proteostatic Programs in Cycling Fibroblast-Lineage Remodeling After Myocardial Ischemic Injury: A Hypothesis Informed by Single-Cell and Spatial Transcriptomics.International journal of molecular sciences · 2026Review
- The Application of Injectable Hydrogels in Myocardial Infarction Repair: Material Design, Biological Functions and Clinical Translation.International journal of molecular sciences · 2026Review
839 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac fibrosis is characterized by net accumulation of extracellular matrix proteins in the cardiac interstitium, and contributes to both systolic and diastolic dysfunction in many cardiac pathophysiologic conditions. This review discusses the cellular effectors and molecular pathways implicated in the pathogenesis of cardiac fibrosis. Although activated myofibroblasts are the main effector cells in the fibrotic heart, monocytes/macrophages, lymphocytes, mast cells, vascular cells and cardiomyocytes may also contribute to the fibrotic response by secreting key fibrogenic mediators. Inflammatory cytokines and chemokines, reactive oxygen species, mast cell-derived proteases, endothelin-1, the renin/angiotensin/aldosterone system, matricellular proteins, and growth factors (such as TGF-β and PDGF) are some of the best-studied mediators implicated in cardiac fibrosis. Both experimental and clinical evidence suggests that cardiac fibrotic alterations may be reversible. Understanding the mechanisms responsible for initiation, progression, and resolution of cardiac fibrosis is crucial to design anti-fibrotic treatment strategies for patients with heart disease.
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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.