ReviewJournal of cardiovascular development and disease2019
Cardiac Fibroblast to Myofibroblast Phenotype Conversion-An Unexploited Therapeutic Target.
Review in Journal of cardiovascular development and disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Emodin for pulmonary fibrosis: a systematic review and meta-analysis of efficacy and molecular mechanisms.Frontiers in medicine · 2025Pooled it
- Natural Products Targeting Myocardial Fibrosis: Pharmacological Basis, Molecular Mechanisms and Translational Barriers.International journal of molecular sciences · 2026Review
- Effects of Stiffness and Degradability on Cardiac Fibroblast Contractility and Extracellular Matrix Secretion in Three-Dimensional Hydrogel Scaffolds.ACS biomaterials science & engineering · 2025Article
- MAPK, PI3K/Akt Pathways, and GSK-3β Activity in Severe Acute Heart Failure in Intensive Care Patients: An Updated Review.Journal of cardiovascular development and disease · 2025Review
- Molecular characterization of suburothelial fibrosis in murine acute recurrent bladder inflammation.Scientific reports · 2025Article
- Dressed in Collagen: 2D and 3D Cardiac Fibrosis Models.International journal of molecular sciences · 2025Review
- From Bench to Bedside: Translational Approaches to Cardiotoxicity in Breast Cancer, Lung Cancer, and Lymphoma Therapies.Cancers · 2025Review
- Albendazole ameliorates aerobic glycolysis in myofibroblasts to reverse pulmonary fibrosis.Journal of translational medicine · 2024Article
- Fibroblast activation protein: Pivoting cancer/chemotherapeutic insight towards heart failure.Biochemical pharmacology · 2024Review
- Cardiac fibrogenesis: an immuno-metabolic perspective.Frontiers in physiology · 2024Review
- Article
- Circular RNA circSMAD4 regulates cardiac fibrosis by targeting miR-671-5p andMolecular therapy. Nucleic acids · 2023Article
- Tissue fibrosis induced by radiotherapy: current understanding of the molecular mechanisms, diagnosis and therapeutic advances.Journal of translational medicine · 2023Review
- Tissue fibrosis induced by radiotherapy: current understanding of the molecular mechanisms, diagnosis and therapeutic advances.Journal of translational medicine · 2023Review
- Treatment of Cardiac Fibrosis with Extracellular Vesicles: What Is Missing for Clinical Translation?International journal of molecular sciences · 2023Review
- Morphological and Functional Remodeling of the Ischemic Heart Correlates with Homocysteine Levels.Journal of cardiovascular development and disease · 2023Article
- Platelet tissue factor pathway inhibitor-α dampens cardiac thrombosis and associated fibrosis in mice.Journal of thrombosis and haemostasis : JTH · 2023Article
- Endothelin-1 Induces Cell Proliferation and Myofibroblast Differentiation through the ETInternational journal of molecular sciences · 2023Article
- Tissue Reactions and Mechanism in Cardiovascular Diseases Induced by Radiation.International journal of molecular sciences · 2022Review
- Inhibition of Wdr5 Attenuates Ang-II-Induced Fibroblast-to-Myofibroblast Transition in Cardiac Fibrosis by Regulating Mdm2/P53/P21 Pathway.Biomolecules · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Fibrosis occurs when the synthesis of extracellular matrix outpaces its degradation, and over time can negatively impact tissue and organ function. In the case of cardiac fibrosis, contraction and relaxation of the heart can be impaired to the point of precipitating heart failure, while at the same time fibrosis can result in arrhythmias due to altered electrical properties of the myocardium. The critical event in the evolution of cardiac fibrosis is the phenotype conversion of cardiac fibroblasts to their overly-active counterparts, myofibroblasts: cells demarked by their expression of novel markers such as periostin, by their gain of contractile activity, and by their pronounced and prolonged increase in the production of extracellular matrix components such as collagens. The phenotype change is dramatic, and can be triggered by many stimuli, including mechanical force, inflammatory cytokines, and growth factors. This review will explore fibroblast to myofibroblast transition mechanisms and will consider the therapeutic potential of targeting this process as a means to arrest or even reverse cardiac fibrosis.
Indexed as
Identifiers
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.