ReviewMatrix biology : journal of the International Society for Matrix Biology2020
Regulators of cardiac fibroblast cell state.
Review in Matrix biology : journal of the International Society for Matrix Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed.
- Selective titin cleavage disrupts cardiac mechanical homeostasis to drive heart failure and fibrosis.Nature cardiovascular research · 2026Article
- Cardiac fibroblasts in myocardial injury and heart failure.European heart journal · 2026Review
- Matrix viscoelasticity regulates dermal fibroblast activation in a three-dimensional fibrillar microenvironment.bioRxiv : the preprint server for biology · 2026Article
- Left ventricular hypertrophy and myocardial fibrosis in heart failure with preserved ejection fraction: mechanisms and treatment.European heart journal · 2026Review
- Cardio-Vascular Extracellular Matrix: The Unmet Enigma.International journal of molecular sciences · 2026Review
- A Proteomics Resource Investigating Fibrosis: Proof-of-Concept for Identifying Novel Drug Candidates.Proteomics · 2026Article
- Orchestrating HFpEF: How Noncoding RNAs Drive Pathophysiology and Phenotypic Outcomes.International journal of molecular sciences · 2025Review
- Mitochondrial Permeability Transition Pore: The Cardiovascular Disease's Molecular Achilles Heel.Biomedicines · 2025Review
- Role of SOX9 in cardiovascular diseases: Evidence today.World journal of cardiology · 2025Review
- Effects of Stiffness and Degradability on Cardiac Fibroblast Contractility and Extracellular Matrix Secretion in Three-Dimensional Hydrogel Scaffolds.ACS biomaterials science & engineering · 2025Article
- Preventing hypocontractility-induced fibroblast expansion alleviates dilated cardiomyopathy.Science (New York, N.Y.) · 2025Article
- A cross-study transcriptional patient map of heart failure defines conserved multicellular coordination in cardiac remodeling.Nature communications · 2025Article
- Junctophilin-2 Regulates Store-Operated Calcium Entry to Drive Cardiac Fibroblast Activation, Fibrotic Repair, and Angiogenesis After Myocardial Infarction.Circulation · 2025Article
- Single-Cell Atlas of the Tricuspid Valve Unveils the Matrifibrocyte-Driven Fibrotic Landscape in Functional Tricuspid Regurgitation.JACC. Asia · 2025Article
- Stress relaxation rates of myocardium from failing and non-failing hearts.Biomechanics and modeling in mechanobiology · 2025Article
- Mitochondrial apoptosis in response to cardiac ischemia-reperfusion injury.Journal of translational medicine · 2025Review
- Hypoxia-inducible factor-2α enhances neutrophil survival to promote cardiac injury following myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2024Article
- Protein kinase N promotes cardiac fibrosis in heart failure by fibroblast-to-myofibroblast conversion.Nature communications · 2024Article
- Exploring Sirtuins: New Frontiers in Managing Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2024Review
- Fibroblast-Specific Depletion of Human Antigen R Alleviates Myocardial Fibrosis Induced by Cardiac Stress.JACC. Basic to translational science · 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.
Funding
Abstract
Fibroblasts are the primary regulator of cardiac extracellular matrix (ECM). In response to disease stimuli cardiac fibroblasts undergo cell state transitions to a myofibroblast phenotype, which underlies the fibrotic response in the heart and other organs. Identifying regulators of fibroblast state transitions would inform which pathways could be therapeutically modulated to tactically control maladaptive extracellular matrix remodeling. Indeed, a deeper understanding of fibroblast cell state and plasticity is necessary for controlling its fate for therapeutic benefit. p38 mitogen activated protein kinase (MAPK), which is part of the noncanonical transforming growth factor β (TGFβ) pathway, is a central regulator of fibroblast to myofibroblast cell state transitions that is activated by chemical and mechanical stress signals. Fibroblast intrinsic signaling, local and global cardiac mechanics, and multicellular interactions individually and synergistically impact these state transitions and hence the ECM, which will be reviewed here in the context of 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.