ArticleMolecular therapy : the journal of the American Society of Gene Therapy2012
AAV9-mediated VEGF-B gene transfer improves systolic function in progressive left ventricular hypertrophy.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 81 citations in OpenAlex.
- AAV Vector Toolkit for the Delivery and Expression of the Artificial microRNA in the Murine Heart.Biotech (Basel (Switzerland)) · 2026Article
- The role of the cardiac lymphatic system in heart failure "reverse remodeling": from developmental signals to druggable targets.Frontiers in immunology · 2026Review
- Global knockout of VEGFB improves lipoprotein lipase activity leading to an improved lipid profile during diabetes.Frontiers in pharmacology · 2026Article
- VEGFR1 as a Target for Cardiovascular Gene Therapy.Journal of cardiovascular translational research · 2025Review
- AAV6 vectors provide superior gene transfer compared to AAV9 vectors following intramyocardial administration.Molecular therapy. Methods & clinical development · 2025Article
- Beneficial effects of vascular endothelial growth factor B gene transfer in the aged heart.Cardiovascular research · 2025Article
- VEGF-B is a novel mediator of ER stress which induces cardiac angiogenesis via RGD-binding integrins independent of VEGFR1/NRP activities.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Morphometric and Molecular Interplay in Hypertension-Induced Cardiac Remodeling with an Emphasis on the Potential Therapeutic Implications.International journal of molecular sciences · 2025Review
- Mast cells: a novel therapeutic avenue for cardiovascular diseases?Cardiovascular research · 2024Review
- Chondroitin polymerizing factor promotes development and progression of colorectal cancer via facilitating transcription of VEGFB.Journal of cellular and molecular medicine · 2024Article
- Role of circulating CD14++CD16Heliyon · 2023Article
- Regulation and impact of cardiac lymphangiogenesis in pressure-overload-induced heart failure.Cardiovascular research · 2023Article
- Role of Lymphangiogenesis in Cardiac Repair and Regeneration.Methodist DeBakey cardiovascular journal · 2023Review
- Therapeutic Potential of VEGF-B in Coronary Heart Disease and Heart Failure: Dream or Vision?Cells · 2022Review
- AAV2-VEGF-B gene therapy failed to induce angiogenesis in ischemic porcine myocardium due to inflammatory responses.Gene therapy · 2022Article
- Knockdown of VEGFB/VEGFR1 Signaling Promotes White Adipose Tissue Browning and Skeletal Muscle Development.International journal of molecular sciences · 2022Article
- Review
- A human cell atlas of the pressure-induced hypertrophic heart.Nature cardiovascular research · 2022Article
- VEGFB Promotes Myoblasts Proliferation and Differentiation through VEGFR1-PI3K/Akt Signaling Pathway.International journal of molecular sciences · 2021Article
- Recent Advances in Gene Therapy for Cardiac Tissue Regeneration.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Mechanisms of the transition from compensatory hypertrophy to heart failure are poorly understood and the roles of vascular endothelial growth factors (VEGFs) in this process have not been fully clarified. We determined the expression profile of VEGFs and relevant receptors during the progression of left ventricular hypertrophy (LVH). C57BL mice were exposed to transversal aortic constriction (TAC) and the outcome was studied at different time points (1 day, 2, 4, and 10 weeks). A clear compensatory phase (2 weeks after TAC) was seen with following heart failure (4 weeks after TAC). Interestingly, VEGF-C and VEGF-D as well as VEGF receptor-3 (VEGFR-3) were upregulated in the compensatory hypertrophy and VEGF-B was downregulated in the heart failure. After treatment with adeno-associated virus serotype 9 (AAV9)-VEGF-B(186) gene therapy in the compensatory phase for 4 weeks the function of the heart was preserved due to angiogenesis, inhibition of apoptosis, and promotion of cardiomyocyte proliferation. Also, the genetic programming towards fetal gene expression, a known phenomenon in heart failure, was partly reversed in AAV9-VEGF-B(186)-treated mice. We conclude that VEGF-C and VEGF-D are associated with the compensatory LVH and that AAV9-VEGF-B(186) gene transfer can rescue the function of the failing heart and postpone the transition towards heart failure.
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Registered trials
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