ArticleThe Journal of clinical investigation2014
Cardiac fibroblasts in pressure overload hypertrophy: the enemy within?
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed.
- Cardiac fibroblast heterogeneity in cardiac fibrosis implication for cell-type-specific treatment.Frontiers in physiology · 2026Review
- Matrisome remodeling in the myocardium of hypertrophic cardiomyopathy; novel targets for molecular diagnostics.Frontiers in cell and developmental biology · 2025Review
- Fibroblasts under pressure: cardiac fibroblast responses to hypertension and antihypertensive therapies.American journal of physiology. Heart and circulatory physiology · 2024Review
- Fibroblast activation protein: Pivoting cancer/chemotherapeutic insight towards heart failure.Biochemical pharmacology · 2024Review
- Fibroblast-specific IKK-β deficiency ameliorates angiotensin II-induced adverse cardiac remodeling in mice.JCI insight · 2021Article
- Review
- Epigenetic Repression of Chloride Channel Accessory 2 Transcription in Cardiac Fibroblast: Implication in Cardiac Fibrosis.Frontiers in cell and developmental biology · 2021Article
- Immunohistochemistry of Kidney a-SMA, Collagen 1, and Collagen 3, in A Novel Mouse Model of Reno-cardiac Syndrome.Bio-protocol · 2020Article
- Regional variations in ex-vivo diffusion tensor anisotropy are associated with cardiomyocyte remodeling in rats after left ventricular pressure overload.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2020Article
- Lack of Thy1 defines a pathogenic fraction of cardiac fibroblasts in heart failure.Biomaterials · 2020Article
- Coronary Microcirculation in Aortic Stenosis.Circulation. Cardiovascular interventions · 2019Review
- Biomarkers for the identification of cardiac fibroblast and myofibroblast cells.Heart failure reviews · 2019Review
- A novel model of reno-cardiac syndrome in the C57BL/ 6 mouse strain.BMC nephrology · 2018Article
- Entanglement of GSK-3β, β-catenin and TGF-β1 signaling network to regulate myocardial fibrosis.Journal of molecular and cellular cardiology · 2017Review
- Age-dependent functional crosstalk between cardiac fibroblasts and cardiomyocytes in a 3D engineered cardiac tissue.Acta biomaterialia · 2017Article
- Transmural gradients of myocardial structure and mechanics: Implications for fiber stress and strain in pressure overload.Progress in biophysics and molecular biology · 2016Review
- Inscribing Optical Excitability to Non-Excitable Cardiac Cells: Viral Delivery of Optogenetic Tools in Primary Cardiac Fibroblasts.Methods in molecular biology (Clifton, N.J.) · 2016Article
- Celecoxib prevents pressure overload-induced cardiac hypertrophy and dysfunction by inhibiting inflammation, apoptosis and oxidative stress.Journal of cellular and molecular medicine · 2016Article
- Endocardial fibroelastosis is caused by aberrant endothelial to mesenchymal transition.Circulation research · 2015Article
- Animal Models to Study Links between Cardiovascular Disease and Renal Failure and Their Relevance to Human Pathology.Frontiers in immunology · 2015Review
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1 author.
Funding
Abstract
Cardiac fibroblasts have been long recognized as active participants in heart disease; however, their exact physiological and pathological roles remain elusive, mainly due to the lack of specific markers. In this issue of the JCI, Moore-Morris and colleagues used a fibroblast-specific collagen1a1-GFP reporter to demonstrate that fibroblast accumulation after aortic banding in murine hearts arises almost exclusively from proliferation of resident fibroblasts originating from both the epicardium and a previously unrecognized source, the endocardium. Further characterization of fibroblast origin and function in different types and stages of heart disease could lead to development of improved fibroblast-targeted cardiac therapies.
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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.