Endothelial Cell Metabolism in Normal and Diseased Vasculature
Higher organisms rely on a closed cardiovascular circulatory system with blood vessels supplying vital nutrients and oxygen to distant tissues. Not surprisingly, vascular pathologies rank among the most life-threatening diseases. At the crux of most of these vascular pathologies are (dysfunctional)...
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| Published in | Circulation research Vol. 116; no. 7; pp. 1231 - 1244 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Heart Association, Inc
27.03.2015
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Higher organisms rely on a closed cardiovascular circulatory system with blood vessels supplying vital nutrients and oxygen to distant tissues. Not surprisingly, vascular pathologies rank among the most life-threatening diseases. At the crux of most of these vascular pathologies are (dysfunctional) endothelial cells (ECs), the cells lining the blood vessel lumen. ECs display the remarkable capability to switch rapidly from a quiescent state to a highly migratory and proliferative state during vessel sprouting. This angiogenic switch has long been considered to be dictated by angiogenic growth factors (eg, vascular endothelial growth factor) and other signals (eg, Notch) alone, but recent findings show that it is also driven by a metabolic switch in ECs. Furthermore, these changes in metabolism may even override signals inducing vessel sprouting. Here, we review how EC metabolism differs between the normal and dysfunctional/diseased vasculature and how it relates to or affects the metabolism of other cell types contributing to the pathology. We focus on the biology of ECs in tumor blood vessel and diabetic ECs in atherosclerosis as examples of the role of endothelial metabolism in key pathological processes. Finally, current as well as unexplored EC metabolism-centric therapeutic avenues are discussed. |
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| AbstractList | Higher organisms rely on a closed cardiovascular circulatory system with blood vessels supplying vital nutrients and oxygen to distant tissues. Not surprisingly, vascular pathologies rank among the most life-threatening diseases. At the crux of most of these vascular pathologies are (dysfunctional) endothelial cells (ECs), the cells lining the blood vessel lumen. ECs display the remarkable capability to switch rapidly from a quiescent state to a highly migratory and proliferative state during vessel sprouting. This angiogenic switch has long been considered to be dictated by angiogenic growth factors (eg, vascular endothelial growth factor) and other signals (eg, Notch) alone, but recent findings show that it is also driven by a metabolic switch in ECs. Furthermore, these changes in metabolism may even override signals inducing vessel sprouting. Here, we review how EC metabolism differs between the normal and dysfunctional/diseased vasculature and how it relates to or affects the metabolism of other cell types contributing to the pathology. We focus on the biology of ECs in tumor blood vessel and diabetic ECs in atherosclerosis as examples of the role of endothelial metabolism in key pathological processes. Finally, current as well as unexplored EC metabolism-centric therapeutic avenues are discussed.Higher organisms rely on a closed cardiovascular circulatory system with blood vessels supplying vital nutrients and oxygen to distant tissues. Not surprisingly, vascular pathologies rank among the most life-threatening diseases. At the crux of most of these vascular pathologies are (dysfunctional) endothelial cells (ECs), the cells lining the blood vessel lumen. ECs display the remarkable capability to switch rapidly from a quiescent state to a highly migratory and proliferative state during vessel sprouting. This angiogenic switch has long been considered to be dictated by angiogenic growth factors (eg, vascular endothelial growth factor) and other signals (eg, Notch) alone, but recent findings show that it is also driven by a metabolic switch in ECs. Furthermore, these changes in metabolism may even override signals inducing vessel sprouting. Here, we review how EC metabolism differs between the normal and dysfunctional/diseased vasculature and how it relates to or affects the metabolism of other cell types contributing to the pathology. We focus on the biology of ECs in tumor blood vessel and diabetic ECs in atherosclerosis as examples of the role of endothelial metabolism in key pathological processes. Finally, current as well as unexplored EC metabolism-centric therapeutic avenues are discussed. Higher organisms rely on a closed cardiovascular circulatory system with blood vessels supplying vital nutrients and oxygen to distant tissues. Not surprisingly, vascular pathologies rank among the most life-threatening diseases. At the crux of most of these vascular pathologies are (dysfunctional) endothelial cells (ECs), the cells lining the blood vessel lumen. ECs display the remarkable capability to switch rapidly from a quiescent state to a highly migratory and proliferative state during vessel sprouting. This angiogenic switch has long been considered to be dictated by angiogenic growth factors (eg, vascular endothelial growth factor) and other signals (eg, Notch) alone, but recent findings show that it is also driven by a metabolic switch in ECs. Furthermore, these changes in metabolism may even override signals inducing vessel sprouting. Here, we review how EC metabolism differs between the normal and dysfunctional/diseased vasculature and how it relates to or affects the metabolism of other cell types contributing to the pathology. We focus on the biology of ECs in tumor blood vessel and diabetic ECs in atherosclerosis as examples of the role of endothelial metabolism in key pathological processes. Finally, current as well as unexplored EC metabolism-centric therapeutic avenues are discussed. Higher organisms rely on a closed cardiovascular circulatory system with blood vessels supplying vital nutrients and oxygen to distant tissues. Not surprisingly, vascular pathologies rank among the most life-threatening diseases. At the crux of most of these vascular pathologies are (dysfunctional) endothelial cells (ECs), the cells lining the blood vessel lumen. ECs display the remarkable capability to switch rapidly from a quiescent state to a highly migratory and proliferative state during vessel sprouting. This angiogenic switch has long been considered to be dictated by angiogenic growth factors ( eg vascular endothelial growth factor; VEGF) and other signals ( eg Notch) alone, but recent findings show that it is also driven by a metabolic switch in ECs. Furthermore, these changes in metabolism may even override signals inducing vessel sprouting. Here, we review how EC metabolism differs between the normal and dysfunctional/diseased vasculature and how it relates to or impacts the metabolism of other cell types contributing to the pathology. We focus on the biology of ECs in tumor blood vessel and diabetic ECs in atherosclerosis as examples of the role of endothelial metabolism in key pathological processes. Finally, current as well as unexplored ‘EC metabolism’-centric therapeutic avenues are discussed. |
| Author | Simons, Michael Eelen, Guy Carmeliet, Peter de Zeeuw, Pauline |
| AuthorAffiliation | From the Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, Department of Oncology, KU Leuven, Leuven, Belgium (G.E., P.d.Z., P.C.); Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, VIB, Leuven, Belgium (G.E., P.d.Z., P.C.); Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, New Haven, CT (M.S.); and Department of Cell Biology, Yale University School of Medicine, New Haven, CT (M.S.) |
| AuthorAffiliation_xml | – name: From the Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, Department of Oncology, KU Leuven, Leuven, Belgium (G.E., P.d.Z., P.C.); Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, VIB, Leuven, Belgium (G.E., P.d.Z., P.C.); Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, New Haven, CT (M.S.); and Department of Cell Biology, Yale University School of Medicine, New Haven, CT (M.S.) – name: 4 Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06520, USA – name: 3 Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, New Haven, CT 06520, USA – name: 1 Laboratory of Angiogenesis and Neurovascular link, Vesalius Research Center, Department of Oncology, University of Leuven, Leuven, B-3000, Belgium – name: 2 Laboratory of Angiogenesis and Neurovascular link, Vesalius Research Center, VIB, Leuven, B-3000, Belgium |
| Author_xml | – sequence: 1 givenname: Guy surname: Eelen fullname: Eelen, Guy organization: From the Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, Department of Oncology, KU Leuven, Leuven, Belgium (G.E., P.d.Z., P.C.); Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, VIB, Leuven, Belgium (G.E., P.d.Z., P.C.); Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, New Haven, CT (M.S.); and Department of Cell Biology, Yale University School of Medicine, New Haven, CT (M.S.) – sequence: 2 givenname: Pauline surname: de Zeeuw fullname: de Zeeuw, Pauline – sequence: 3 givenname: Michael surname: Simons fullname: Simons, Michael – sequence: 4 givenname: Peter surname: Carmeliet fullname: Carmeliet, Peter |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25814684$$D View this record in MEDLINE/PubMed |
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| Copyright | 2015 American Heart Association, Inc. |
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| Keywords | atherosclerosis cancer diabetes mellitus endothelial metabolism angiogenesis |
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| SubjectTerms | Amino Acids - metabolism Atherosclerosis - metabolism Atherosclerosis - pathology Cell Movement Diabetic Angiopathies - metabolism Endothelial Cells - classification Endothelial Cells - metabolism Endothelial Cells - pathology Endothelium, Vascular - metabolism Energy Metabolism Fatty Acids - metabolism Glucose - metabolism Glycation End Products, Advanced - metabolism Humans Morphogenesis Neoplasms - blood supply Neovascularization, Pathologic - metabolism Neovascularization, Physiologic - physiology Nitric Oxide - metabolism Oxidative Stress Reactive Oxygen Species - metabolism Stromal Cells - metabolism Translational Research, Biomedical Tumor Microenvironment Vascular Diseases - metabolism Vascular Diseases - pathology |
| Title | Endothelial Cell Metabolism in Normal and Diseased Vasculature |
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