ArticleCirculation2018
Bone Morphogenetic Protein 9 Reduces Cardiac Fibrosis and Improves Cardiac Function in Heart Failure.
Article in Circulation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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Who cites it
54 citing papers in PubMed, 84 citations in OpenAlex.
- Deciphering the Genetic Underpinnings of Liver Cirrhosis-Heart Failure Comorbidity Through Multi-Omics: CRIM1 as a Key Endothelial Mediator.International journal of molecular sciences · 2026Article
- Conserved Transcriptional Circuits Regulate Cardiac Fibroblast-Mediated Fibrosis.Circulation research · 2026Article
- Pulpitis Transiently Affect Hepatic Bone Morphogenetic Protein 9 Expression by Lipopolysaccharide.International dental journal · 2026Article
- BMP7 attenuates myocardial injury and preserves cardiac function after myocardial infarction by inhibiting cardiomyocyte pyroptosis.Apoptosis : an international journal on programmed cell death · 2026Article
- Bone morphogenetic protein (BMP)-9, a systemic homeostasis factor with diverse functions in the liver and beyond.Bioscience reports · 2025Review
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- Restoring Prostacyclin/PGI2-PTGIR signaling alleviates intestinal fibrosis in Crohn's disease via fibroblast-specific YAP/TAZ inhibition.Journal of Crohn's & colitis · 2025Article
- The Association of Circulating Bone Morphogenetic Protein 9 and Arterial Stiffness in Hypertensive Patients.Journal of clinical hypertension (Greenwich, Conn.) · 2025Article
- Complex regulation of cardiac fibrosis: insights from immune cells and signaling pathways.Journal of translational medicine · 2025Review
- LMK235 ameliorates inflammation and fibrosis after myocardial infarction by inhibiting LSD1-related pathway.Scientific reports · 2024Article
- Emerging role of BMPs/BMPR2 signaling pathway in treatment for pulmonary fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Review
- BMP2 Diminishes Angiotensin II-Induced Atrial Fibrillation by Inhibiting NLRP3 Inflammasome Signaling in Atrial Fibroblasts.Biomolecules · 2024Article
- Estrogen inhibits TGF‑β1‑stimulated cardiac fibroblast differentiation and collagen synthesis by promoting Cdc42.Molecular medicine reports · 2024Article
- ALK1 Deficiency Impairs the Wound-Healing Process and Increases Mortality in Murine Model of Myocardial Infarction.Journal of cardiovascular translational research · 2024Article
- Hydrogels for Cardio and Vascular Tissue Repair and Regeneration.Gels (Basel, Switzerland) · 2024Review
- ALK1 Signaling in Human Cardiac Progenitor Cells Promotes a Pro-angiogenic Secretome.Journal of cellular signaling · 2024Article
- Integrative Single-Cell Analysis of Cardiomyopathy Identifies Differences in Cell Stemness and Transcriptional Regulatory Networks among Fibroblast Subpopulations.Cardiology research and practice · 2024Article
- Quality Over Quantity: BMP-9 Regulation of Scar Formation After Myocardial Infarction.JACC. Basic to translational science · 2023Article
- Loss of Bone Morphogenetic Protein-9 Reduces Survival and Increases MMP Activity After Myocardial Infarction.JACC. Basic to translational science · 2023Article
- Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHeart failure is a growing cause of morbidity and mortality worldwide. Transforming growth factor beta (TGF-β1) promotes cardiac fibrosis, but also activates counterregulatory pathways that serve to regulate TGF-β1 activity in heart failure. Bone morphogenetic protein 9 (BMP9) is a member of the TGFβ family of cytokines and signals via the downstream effector protein Smad1. Endoglin is a TGFβ coreceptor that promotes TGF-β1 signaling via Smad3 and binds BMP9 with high affinity. We hypothesized that BMP9 limits cardiac fibrosis by activating Smad1 and attenuating Smad3, and, furthermore, that neutralizing endoglin activity promotes BMP9 activity.
methodsWe examined BMP9 expression and signaling in human cardiac fibroblasts and human subjects with heart failure. We used the transverse aortic constriction-induced model of heart failure to evaluate the functional effect of BMP9 signaling on cardiac remodeling.
resultsBMP9 expression is increased in the circulation and left ventricle (LV) of human subjects with heart failure and is expressed by cardiac fibroblasts. Next, we observed that BMP9 attenuates type I collagen synthesis in human cardiac fibroblasts using recombinant human BMP9 and a small interfering RNA approach. In BMP9
conclusionsOur results identify a novel functional role for BMP9 as an endogenous inhibitor of cardiac fibrosis attributable to LV pressure overload and further show that treatment with either recombinant BMP9 or disruption of endoglin activity promotes BMP9 activity and limits cardiac fibrosis in heart failure, thereby providing potentially novel therapeutic approaches for patients with 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.