ArticleEMBO molecular medicine2014
VEGF-B-induced vascular growth leads to metabolic reprogramming and ischemia resistance in the heart.
Article in EMBO molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
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Who cites it
95 citing papers in PubMed, 169 citations in OpenAlex.
- Vascular and musculoskeletal interactions: structure, function, and therapeutic strategies for sarcopenia and osteoporosis.MedScience · 2026Review
- Predictive value of miR-193a-5p combined with VEGFB in the diagnosis and prognosis of CHD.Journal of cardiothoracic surgery · 2026Article
- Gene Therapy for Heart Failure.Journal of cardiovascular translational research · 2026Review
- Caught in the crossfire: cardiac complications of cancer therapy.The Journal of clinical investigation · 2026Review
- High Burden of Premature Ventricular Contractions Upregulates Transcriptional Markers of Inflammation and Promotes Adverse Cardiac Remodeling Linked to Cardiomyopathy.Circulation. Arrhythmia and electrophysiology · 2026Article
- Global knockout of VEGFB improves lipoprotein lipase activity leading to an improved lipid profile during diabetes.Frontiers in pharmacology · 2026Article
- Endothelial cell metabolism in cardiovascular physiology and disease.Nature reviews. Cardiology · 2025Review
- Characterization of anticancer therapy-induced microvascular dysfunction in patients with breast cancer supports targeted intervention.JCI insight · 2025Article
- Beneficial effects of vascular endothelial growth factor B gene transfer in the aged heart.Cardiovascular research · 2025Article
- Fenofibrate Differently Affects the Heart's Morphology and Metabolism in Young and Old Rats.International journal of molecular sciences · 2025Article
- Multifunctional MOF microneedle patch with adsorbed exosomes for enhanced diabetic wound healing.Materials today. Bio · 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
- Vascular endothelial growth factor signaling in health and disease: from molecular mechanisms to therapeutic perspectives.Signal transduction and targeted therapy · 2025Review
- LncRNA Growth Arrest Specific 5 Promotes Glucose Metabolism Reprogramming Via the IGF2BP1/SIX1 Axis and Inhibits Ferroptosis of Endothelial Progenitor Cells Via the miR-23a-3p/SLC7A11 Axis in Coronary Heart Disease.Anatolian journal of cardiology · 2025Article
- Shikimic acid protects against doxorubicin-induced cardiotoxicity in rats.Scientific reports · 2025Article
- Exploring glycolytic enzymes in disease: potential biomarkers and therapeutic targets in neurodegeneration, cancer and parasitic infections.Open biology · 2025Review
- Leptin drives glucose metabolism to promote cardiac protection via OPA1-mediated HDAC5 translocation and Glut4 transcription.Functional & integrative genomics · 2025Article
- Possibility of Using NO Modulators for Pharmacocorrection of Endothelial Dysfunction After Prenatal Hypoxia.Pharmaceuticals (Basel, Switzerland) · 2025Article
- flt1 inactivation promotes zebrafish cardiac regeneration by enhancing endothelial activity and limiting the fibrotic response.Development (Cambridge, England) · 2024Article
- Soluble FLT-1 in angiogenesis: pathophysiological roles and therapeutic implications.Angiogenesis · 2024Review
35 more citing papers are in PubMed but not listed here.
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Authors and funding
20 authors at 9 institutions in 4 countries.
Funding
Abstract
Angiogenic growth factors have recently been linked to tissue metabolism. We have used genetic gain- and loss-of function models to elucidate the effects and mechanisms of action of vascular endothelial growth factor-B (VEGF-B) in the heart. A cardiomyocyte-specific VEGF-B transgene induced an expanded coronary arterial tree and reprogramming of cardiomyocyte metabolism. This was associated with protection against myocardial infarction and preservation of mitochondrial complex I function upon ischemia-reperfusion. VEGF-B increased VEGF signals via VEGF receptor-2 to activate Erk1/2, which resulted in vascular growth. Akt and mTORC1 pathways were upregulated and AMPK downregulated, readjusting cardiomyocyte metabolic pathways to favor glucose oxidation and macromolecular biosynthesis. However, contrasting with a previous theory, there was no difference in fatty acid uptake by the heart between the VEGF-B transgenic, gene-targeted or wildtype rats. Importantly, we also show that VEGF-B expression is reduced in human heart disease. Our data indicate that VEGF-B could be used to increase the coronary vasculature and to reprogram myocardial metabolism to improve cardiac function in ischemic heart disease.
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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.