Suppression of accelerated diabetic atherosclerosis by the soluble receptor for advanced glycation endproducts
Accelerated atherosclerosis in patients with diabetes is a major cause of their morbidity and mortality, and it is unresponsive to therapy aimed at restoring relative euglycemia. In hyperglycemia, nonenzymatic glycation and oxidation of proteins and lipids results in the accumulation of irreversibly...
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| Published in | Nature medicine Vol. 4; no. 9; pp. 1025 - 1031 |
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| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
01.09.1998
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Accelerated atherosclerosis in patients with diabetes is a major cause of their morbidity and mortality, and it is unresponsive to therapy aimed at restoring relative euglycemia. In hyperglycemia, nonenzymatic glycation and oxidation of proteins and lipids results in the accumulation of irreversibly formed advanced glycation endproducts. These advanced glycation endproducts engage their receptor in cells of the blood vessel wall, thereby activating mechanisms linked to the development of vascular lesions. We report here a model of accelerated and advanced atherosclerosis in diabetic mice deficient for apolipoprotein E. Treatment of these mice with the soluble extracellular domain of the receptor for advanced glycation endproducts completely suppressed diabetic atherosclerosis in a glycemia- and lipid-independent manner. These findings indicate interaction between the advanced glycation endproducts and their receptor is involved in the development of accelerated atherosclerosis in diabetes, and identify this receptor as a new therapeutic target in diabetic macrovascular disease. |
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| AbstractList | Accelerated atherosclerosis in patients with diabetes is a major cause of their morbidity and mortality, and it is unresponsive to therapy aimed at restoring relative euglycemia. In hyperglycemia, nonenzymatic glycation and oxidation of proteins and lipids results in the accumulation of irreversibly formed advanced glycation endproducts. These advanced glycation endproducts engage their receptor in cells of the blood vessel wall, thereby activating mechanisms linked to the development of vascular lesions. We report here a model of accelerated and advanced atherosclerosis in diabetic mice deficient for apolipoprotein E. Treatment of these mice with the soluble extracellular domain of the receptor for advanced glycation endproducts completely suppressed diabetic atherosclerosis in a glycemia- and lipid-independent manner. These findings indicate interaction between the advanced glycation endproducts and their receptor is involved in the development of accelerated atherosclerosis in diabetes, and identify this receptor as a new therapeutic target in diabetic macrovascular disease. |
| Author | Schmidt, Ann Marie Lu, Yan Chow, Wing Sun Park, Lisa Stern, David Raman, Kathleen G Lee, Kenneth J Ferran, Luis J |
| Author_xml | – sequence: 1 givenname: Ann Marie surname: Schmidt fullname: Schmidt, Ann Marie organization: Division of Surgical Science, Department of Surgery, Columbia University College of Physicians and Surgeons Department of Medicine Columbia University College of Physicians and Surgeons – sequence: 2 givenname: Lisa surname: Park fullname: Park, Lisa organization: Division of Surgical Science, Department of Surgery, Columbia University College of Physicians and Surgeons Department of Physiology Columbia University College of Physicians and Surgeons – sequence: 3 givenname: Kathleen G surname: Raman fullname: Raman, Kathleen G organization: Division of Surgical Science, Department of Surgery, Columbia University College of Physicians and Surgeons Department of Physiology Columbia University College of Physicians and Surgeons – sequence: 4 givenname: Kenneth J surname: Lee fullname: Lee, Kenneth J organization: Division of Surgical Science, Department of Surgery, Columbia University College of Physicians and Surgeons Department of Physiology Columbia University College of Physicians and Surgeons – sequence: 5 givenname: Yan surname: Lu fullname: Lu, Yan organization: Division of Surgical Science, Department of Surgery, Columbia University College of Physicians and Surgeons Department of Physiology Columbia University College of Physicians and Surgeons – sequence: 6 givenname: Luis J surname: Ferran fullname: Ferran, Luis J organization: Division of Surgical Science, Department of Surgery, Columbia University College of Physicians and Surgeons Department of Physiology Columbia University College of Physicians and Surgeons – sequence: 7 givenname: Wing Sun surname: Chow fullname: Chow, Wing Sun organization: Division of Surgical Science, Department of Surgery, Columbia University College of Physicians and Surgeons Department of Physiology Columbia University College of Physicians and Surgeons – sequence: 8 givenname: David surname: Stern fullname: Stern, David organization: Division of Surgical Science, Department of Surgery, Columbia University College of Physicians and Surgeons Department of Physiology Columbia University College of Physicians and Surgeons |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/9734395$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Animals Arteriosclerosis - drug therapy Arteriosclerosis - etiology Cell Line Diabetes Mellitus, Experimental - complications Diabetes Mellitus, Experimental - physiopathology Diabetic Angiopathies - drug therapy Glycation End Products, Advanced - metabolism Humans Male Mice Mice, Inbred C57BL Receptor for Advanced Glycation End Products Receptors, Immunologic - metabolism Receptors, Immunologic - therapeutic use Recombinant Fusion Proteins - metabolism Solubility Spodoptera Streptozocin |
| Title | Suppression of accelerated diabetic atherosclerosis by the soluble receptor for advanced glycation endproducts |
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