Cardiovascular disease in diabetes, beyond glucose
Despite the decades-old knowledge that diabetes mellitus is a major risk factor for cardiovascular disease, the reasons for this association are only partially understood. While this association is true for both type 1 and type 2 diabetes, different pathophysiological processes may be responsible. L...
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Published in | Cell metabolism Vol. 33; no. 8; pp. 1519 - 1545 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
03.08.2021
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Subjects | |
Online Access | Get full text |
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Summary: | Despite the decades-old knowledge that diabetes mellitus is a major risk factor for cardiovascular disease, the reasons for this association are only partially understood. While this association is true for both type 1 and type 2 diabetes, different pathophysiological processes may be responsible. Lipids and other risk factors are indeed important, whereas the role of glucose is less clear. This lack of clarity stems from clinical trials that do not unambiguously show that intensive glycemic control reduces cardiovascular events. Animal models have provided mechanisms that link diabetes to increased atherosclerosis, and evidence consistent with the importance of factors beyond hyperglycemia has emerged. We review clinical, pathological, and animal studies exploring the pathogenesis of atherosclerosis in humans living with diabetes and in mouse models of diabetes. An increased effort to identify risk factors beyond glucose is now needed to prevent the increased cardiovascular disease risk associated with diabetes.
Diabetes increases cardiovascular disease risk, but the reasons for the association are not fully understood. Here, Eckel et al. review clinical and animal studies that explore the pathogenesis of atherosclerosis in the diabetes context. They discuss the need to identify and understand risk factors beyond glucose in order to prevent increased cardiovascular disease risk in diabetes. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 |
ISSN: | 1550-4131 1932-7420 1932-7420 |
DOI: | 10.1016/j.cmet.2021.07.001 |