Why Atherosclerotic Plaques Are More Dangerous in Type 2 Diabetes? Study Sheds Light
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Researchers at Lund University Diabetes Centre, have led a study that has mapped out differences in the atherosclerotic process in people who have type 2 diabetes and in people who do not have the disease. The study has now been published in Nature Communications.
"A stroke or heart attack often leads to reduced quality of life and, in the worst-case scenario, death. Since we know that people with type 2 diabetes have a higher risk of being affected, we set particularly ambitious treatment goals for patients with atherosclerosis and type 2 diabetes. Current treatment options mainly target risk factors such as blood lipids, blood pressure and lifestyle, regardless of whether the person has diabetes or not. Our new study provides additional evidence that people with type 2 diabetes may need new treatments that target specific molecular mechanisms of atherosclerosis," says Andreas Edsfeldt, cardiologist and associate professor at Lund University Diabetes Centre.
The researchers have carried out detailed analyses of atherosclerotic plaques from a total of 219 individuals with cardiovascular diseases, and of these, 72 had type 2 diabetes. Atherosclerosis means that fats, cells, calcium and connective tissue have accumulated for a long time on the inside of the arteries, forming what are known as atherosclerotic plaques. The research team found that atherosclerotic plaques from patients with type 2 diabetes had lower levels of protective connective tissue in comparison with plaques from those without diabetes. The reason for this seems to be a lack of a specific growth factor called TGF-beta2. The research team also found that high blood sugar levels can be linked to a reduced ability to form protective connective tissue in the atherosclerotic plaques, which leads to an increased risk of stroke or heart attack.
Reference: Singh, P., Sun, J., Cavalera, M. et al. Dysregulation of MMP2-dependent TGF-ß2 activation impairs fibrous cap formation in type 2 diabetes-associated atherosclerosis. Nat Commun 15, 10464 (2024). https://doi.org/10.1038/s41467-024-50753-8
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