ReviewCells2021
Cardiac Fibrosis and Fibroblasts.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 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
94 citing papers in PubMed, 172 citations in OpenAlex.
- The Role of the Extracellular Volume of the Infarction Zone and the Remote Myocardium in Predicting Systolic Dysfunction After the First Myocardial Infarction.Diagnostics (Basel, Switzerland) · 2026Article
- Mechanics of compression-driven morphogenesis.Development (Cambridge, England) · 2026Review
- From Ischemic Injury to Arrhythmogenic Substrate: Molecular and Histopathological Insights into Post-Infarction Sudden Cardiac Death.Life (Basel, Switzerland) · 2026Review
- Stanniocalcin-1 Attenuates Cardiac Fibrosis Post Ischemia-Reperfusion Injury by Targeting the DOCKER Domain of Dedicator of Cytokinesis 1.Journal of the American Heart Association · 2026Article
- Involvement of Fibulin-5 in endothelial to mesenchymal transition leading to cardiac fibrosis during metabolic syndrome.Journal of translational medicine · 2026Article
- Cell migration inducing protein alleviates adverse cardiac remodelling after ischaemia and reperfusion injury by controlling fibroblast activation.Cardiovascular research · 2026Article
- AhR as a Common Denominator in Immunity and Inflammation in Chronic Lung Diseases: Molecular and Clinical Insights.Diseases (Basel, Switzerland) · 2026Review
- Doxorubicin exposure leads to cardiac fibroblast dysregulation and worsens fibrotic remodeling in the pathological heart.Journal of molecular and cellular cardiology plus · 2026Article
- Plasminogen Activation System and Fibroblasts: Impact on Tissue Remodeling, Disease, and Organ Homeostasis.Inflammation · 2026Review
- Immunometabolism in Cardiac Remodeling: Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Molecular Mechanisms of Cardiac Fibrosis: A Pathologist's Perspective.Current issues in molecular biology · 2026Review
- Ferroptosis in Myocardial Fibrosis: Mechanisms and Therapeutic Insights.Antioxidants (Basel, Switzerland) · 2026Review
- Cardio-Vascular Extracellular Matrix: The Unmet Enigma.International journal of molecular sciences · 2026Review
- Embryonic Mouse Cardiac Fibroblast Isolation.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Dihydroartemisinin alleviates pulmonary fibrosis by modulating the calcium signaling pathway in fibroblasts.Journal of translational medicine · 2025Article
- Left ventricular deformation and tissue characteristics in hypertrophic cardiomyopathy patients with HFpEF: a CMR study.BMC medical imaging · 2025Article
- Factors Released by Polarized Neutrophil-like Cells Modulate Cardiac Fibroblast Phenotype and Limit the Inflammatory Response After Myocardial Infarction.Biomedicines · 2025Article
- Runx1 drives cardiac fibrosis and heart failure through epigenetic activation of myofibroblasts in pressure overload-induced cardiac remodeling.BMC cardiovascular disorders · 2025Article
- Alpinetin Alleviates Cardiac Inflammation and Remodeling via TLR4/MyD88/NF-κB Signaling Pathway in Rats with Acute Myocardial Infarction.International journal of molecular sciences · 2025Article
- The role of CARMA3 in regulating fibrosis to prevent hypertrophic cardiomyopathy.Cell death discovery · 2025Article
34 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
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac fibrosis is the excess deposition of extracellular matrix (ECM), such as collagen. Myofibroblasts are major players in the production of collagen, and are differentiated primarily from resident fibroblasts. Collagen can compensate for the dead cells produced by injury. The appropriate production of collagen is beneficial for preserving the structural integrity of the heart, and protects the heart from cardiac rupture. However, excessive deposition of collagen causes cardiac dysfunction. Recent studies have demonstrated that myofibroblasts can change their phenotypes. In addition, myofibroblasts are found to have functions other than ECM production. Myofibroblasts have macrophage-like functions, in which they engulf dead cells and secrete anti-inflammatory cytokines. Research into fibroblasts has been delayed due to the lack of selective markers for the identification of fibroblasts. In recent years, it has become possible to genetically label fibroblasts and perform sequencing at single-cell levels. Based on new technologies, the origins of fibroblasts and myofibroblasts, time-dependent changes in fibroblast states after injury, and fibroblast heterogeneity have been demonstrated. In this paper, recent advances in fibroblast and myofibroblast research are reviewed.
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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.