ArticleThe American journal of pathology2010
Bone marrow-derived cells contribute to fibrosis in the chronically failing heart.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 98 citations in OpenAlex.
- Circulating Fibrocytes: Cellular Mediators of Tissue Fibrosis.International journal of molecular sciences · 2026Review
- The immune mechanisms of acute exacerbations of idiopathic pulmonary fibrosis.Frontiers in immunology · 2024Review
- A comprehensive review of acute cardio-renal syndrome: need for novel biomarkers.Frontiers in pharmacology · 2023Review
- Clinical effectiveness of second-line antihyperglycemic drugs on major adverse cardiovascular events: An emulation of a target trial.Frontiers in endocrinology · 2023Article
- Non-ischemic dilated cardiomyopathy and cardiac fibrosis.Heart failure reviews · 2021Review
- Cardiac fibrosis.Cardiovascular research · 2021Review
- Chemokines in cardiac fibrosis.Current opinion in physiology · 2021Article
- Tissue factor cytoplasmic domain exacerbates post-infarct left ventricular remodeling via orchestrating cardiac inflammation and angiogenesis.Theranostics · 2021Article
- Innate Immunity Effector Cells as Inflammatory Drivers of Cardiac Fibrosis.International journal of molecular sciences · 2020Review
- IL-18/IL-18R1 promotes circulating fibrocyte differentiation in the aging population.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- DPP4 Inhibition, NPYThe Journal of pharmacology and experimental therapeutics · 2020Article
- Interleukin 4: Its Role in Hypertension, Atherosclerosis, Valvular, and Nonvalvular Cardiovascular Diseases.Journal of cardiovascular pharmacology and therapeutics · 2020Review
- The Effects of DPP-4 Inhibitors, GLP-1RAs, and SGLT-2/1 Inhibitors on Heart Failure Outcomes in Diabetic Patients With and Without Heart Failure History: Insights From CVOTs and Drug Mechanism.Frontiers in endocrinology · 2020Review
- Role of B7H3/IL-33 Signaling in Pulmonary Fibrosis-induced Profibrogenic Alterations in Bone Marrow.American journal of respiratory and critical care medicine · 2019Article
- Fibroblasts and Their Pathological Functions in the Fibrosis of Aortic Valve Sclerosis and Atherosclerosis.Biomolecules · 2019Review
- Correlation between circulating fibrocytes and dermal thickness in limited cutaneous systemic sclerosis patients: a pilot study.Rheumatology international · 2019Article
- CXCR4 Antagonism Reduces Cardiac Fibrosis and Improves Cardiac Performance in Dilated Cardiomyopathy.Frontiers in pharmacology · 2019Article
- Cardiac Fibroblasts and Cardiac Fibrosis: Precise Role of Exosomes.Frontiers in cell and developmental biology · 2019Review
- Extracellular Ubiquitin(1-76) and Ubiquitin(1-74) Regulate Cardiac Fibroblast Proliferation.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Elevated Circulating Fibrocytes Is a Marker of Left Atrial Fibrosis and Recurrence of Persistent Atrial Fibrillation.Journal of the American Heart Association · 2018Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Cardiac fibrosis contributes significantly to the phenotype of the chronically failing heart. It is not clear whether in this setting the fibrosis is contributed by native cardiac fibroblasts or alternatively by recruitment of cells arising from the bone marrow. We aimed to determine the contribution of bone marrow-derived cells to cardiac fibrosis in the failing heart and to investigate potentially contributing cytokines. Bone marrow-derived fibrocyte recruitment to the failing heart was studied in a transgenic (Mst1 mice) model of dilated cardiomyopathy. In conjunction, we examined the role of stromal-derived factor-1 (SDF-1), a key chemoattractant, by assessing myocardial expression and secretion by cardiomyocytes and in clinical samples. Bone marrow-derived cells were recruited in significantly greater numbers in Mst1 versus control mice (P < 0.001), contributing 17 +/- 4% of the total fibroblast load in heart failure. Patients with heart failure had higher plasma levels of SDF-1 than healthy control subjects (P < 0.01). We found that cardiomyocytes constitutively secrete SDF-1, which is significantly up-regulated by angiotensin II. SDF-1 was shown to increases cardiac fibroblast migration by 59% (P < 0.05). Taken together, our data suggest that recruitment of bone marrow-derived cells under the influence of factors, including SDF-1, may play an important role in the pathogenesis of cardiac fibrosis in heart failure.
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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.