Key result
Altered HDL contributes to diabetic cardiomyopathy both indirectly via metabolic triggers and directly via cardiac cellular consequences including inflammation, oxidative stress, and fibrosis.
This review highlights the mechanistic pathways by which altered HDL contributes to the pathogenesis of diabetic cardiomyopathy, suggesting its role beyond traditional atherosclerosis.
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HDL alterations may drive diabetic cardiomyopathy pathogenesis; leaves open whether targeted modulation improves clinical outcomes.
Diabetic cardiopathy includes a specific cardiomyopathy, which occurs in the absence of coronary heart disease and hypertension under diabetes mellitus. Hyperglycemia, hyperinsulinemia, and hyperlipidemia, characteristic metabolic disturbances evident in diabetes mellitus, all three lead to a specific altered cardiac structure and function. Recently, it has been demonstrated that altered HDL, be it low HDL or dysfunctional HDL is not only a consequence of diabetes mellitus, but can also contribute to the development of diabetes mellitus, and therefore also of diabetic cardiomyopathy. This review summarizes how HDL can indirectly affect diabetic cardiomyopathy via their influence on the metabolic triggers hyperglycemia, hyperinsulinemia, and hyperlipidemia, and how they can directly influence the cardiac cellular consequences, typical for diabetic cardiomyopathy, including inflammation, oxidative stress, apoptosis, fibrosis, Ca2+ handling, glucose homeostasis, and endothelial dysfunction.
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Spillmann et al. (2012) conducted a review in Diabetic Cardiomyopathy. Altered HDL was evaluated. Altered HDL contributes to diabetic cardiomyopathy both indirectly via metabolic triggers and directly via cardiac cellular consequences including inflammation, oxidative stress, and fibrosis.
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