ReviewCells2021
Mechanisms of Fibroblast Activation and Myocardial Fibrosis: Lessons Learned from FB-Specific Conditional Mouse Models.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Pooled it
- POU2F1 promotes hypertensive cardiac fibrosis by regulating mitochondrial homeostasis through PINK1/Parkin‑dependent mitophagy.Molecular medicine reports · 2026Article
- Natural Products Targeting Myocardial Fibrosis: Pharmacological Basis, Molecular Mechanisms and Translational Barriers.International journal of molecular sciences · 2026Review
- Engineering autoimmune disease models using organoids: Harnessing microenvironmental engineering for precision medicine and immunological recapitulation.Bioengineering & translational medicine · 2026Review
- BMSCs regulate RGS3 expression in ovarian stromal cells to improve ovarian stromal fibrosis and angiogenic microenvironment in cyclophosphamide-induced premature ovarian failure.Stem cell research & therapy · 2026Article
- Loss of p300/CBP-associated factor aggravates cardiac remodeling via regulation of CAMKK2 acetylation.Experimental & molecular medicine · 2026Article
- Non-invasive Evaluation of Myocardial Fibrosis Using T1 and T2 Mapping by Cardiac Magnetic Resonance Imaging.Cureus · 2026Review
- Cardiac fibroblast heterogeneity in cardiac fibrosis implication for cell-type-specific treatment.Frontiers in physiology · 2026Review
- Single-cell RNA sequencing pseudobulk analysis and machine learning identify candidate biomarkers for ischemic cardiomyopathy.Frontiers in cardiovascular medicine · 2026Article
- The role of different types of programmed cell death in myocardial fibrosis: from mechanisms to therapeutics.Frontiers in cardiovascular medicine · 2026Review
- Fibroblasts as key effectors of acupuncture in treatment of rheumatoid arthritis.Frontiers in immunology · 2026Article
- Amphiregulin in Fibrotic Diseases and Cancer.International journal of molecular sciences · 2025Review
- Morphometric and Molecular Interplay in Hypertension-Induced Cardiac Remodeling with an Emphasis on the Potential Therapeutic Implications.International journal of molecular sciences · 2025Review
- Low-density lipoprotein receptor-related protein 6 ameliorates cardiac hypertrophy by regulating CTSD/HSP90α signaling during pressure overload.Acta pharmacologica Sinica · 2025Article
- Early treatment with nootkatone prevents pressure overload-induced ventricular remodeling and heart failure.Frontiers in pharmacology · 2025Article
- Integrative multi-omics identifies MEIS3 as a diagnostic biomarker and immune modulator in hypertrophic cardiomyopathy.Frontiers in immunology · 2025Article
- Wnt Signaling Inhibitors as Therapeutic Approach in Ischemic Heart Disease.Molecules (Basel, Switzerland) · 2024Review
- Evaluation of the Canonical Wnt Signaling Pathway in the Hearts of Hypertensive Rats of Various Etiologies.International journal of molecular sciences · 2024Article
- In Vitro Assessment of Cardiac Fibroblast Activation at Physiologic Stiffness.Current protocols · 2024Article
- In Vitro Mechanical Stimulation to Reproduce the Pathological Hallmarks of Human Cardiac Fibrosis on a Beating Chip and Predict The Efficacy of Drugs and Advanced Therapies.Advanced healthcare materials · 2024Article
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
Heart failure (HF) is a leading cause of morbidity and mortality across the world. Cardiac fibrosis is associated with HF progression. Fibrosis is characterized by the excessive accumulation of extracellular matrix components. This is a physiological response to tissue injury. However, uncontrolled fibrosis leads to adverse cardiac remodeling and contributes significantly to cardiac dysfunction. Fibroblasts (FBs) are the primary drivers of myocardial fibrosis. However, until recently, FBs were thought to play a secondary role in cardiac pathophysiology. This review article will present the evolving story of fibroblast biology and fibrosis in cardiac diseases, emphasizing their recent shift from a supporting to a leading role in our understanding of the pathogenesis of cardiac diseases. Indeed, this story only became possible because of the emergence of FB-specific mouse models. This study includes an update on the advancements in the generation of FB-specific mouse models. Regarding the underlying mechanisms of myocardial fibrosis, we will focus on the pathways that have been validated using FB-specific, in vivo mouse models. These pathways include the TGF-β/SMAD3, p38 MAPK, Wnt/β-Catenin, G-protein-coupled receptor kinase (GRK), and Hippo signaling. A better understanding of the mechanisms underlying fibroblast activation and fibrosis may provide a novel therapeutic target for the management of adverse fibrotic remodeling in the diseased heart.
Indexed as
Identifiers
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.