Endothelial cell-cardiomyocyte crosstalk in diabetic cardiomyopathy.
The incidence of diabetes is increasing globally, with cardiovascular disease accounting for a substantial number of diabetes-related deaths. Although atherosclerotic vascular disease is a primary reason for this cardiovascular dysfunction, heart failure in patients with diabetes might also be an outcome of an intrinsic heart muscle malfunction, labelled diabetic cardiomyopathy. Changes in cardiomyocyte metabolism, which encompasses a shift to exclusive fatty acid utilization, are considered a leading stimulus for this cardiomyopathy. In addition to cardiomyocytes, endothelial cells (ECs) make up a significant proportion of the heart, with the majority of ATP generation in these cells provided by glucose. In this review, we will discuss the metabolic machinery that drives energy metabolism in the cardiomyocyte and EC, its breakdown following diabetes, and the research direction necessary to assist in devising novel therapeutic strategies to prevent or delay diabetic heart disease.
Faculty of Pharmaceutical Sciences, The University of British Columbia, 2405 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3.
Andrea
A
Wan
Faculty of Pharmaceutical Sciences, The University of British Columbia, 2405 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3 rodrigue@interchange.ubc.ca.
Brian
B
Rodrigues
D000255:Adenosine Triphosphate / Q000378:metabolism; D020533:Angiogenesis Inhibitors / Q000627:therapeutic use; D000818:Animals; D002450:Cell Communication / Q000187:drug effects; D058065:Diabetic Cardiomyopathies / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D004734:Energy Metabolism / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D005227:Fatty Acids / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D005966:Glucuronidase / Q000378:metabolism; D006801:Humans; D008071:Lipoprotein Lipase / Q000378:metabolism; D058990:Molecular Targeted Therapy; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D015398:Signal Transduction; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors / Q000378:metabolism; D000099175:Heparanase
D000255:Adenosine Triphosphate; D020533:Angiogenesis Inhibitors; D004791:Enzyme Inhibitors; D005227:Fatty Acids; D005947:Glucose; D005966:Glucuronidase; D008071:Lipoprotein Lipase; D042461:Vascular Endothelial Growth Factor A; D000099175:Heparanase
Cardiomyocyte metabolism; Endothelial cell metabolism; Heparanase; Lipoprotein lipase; Vascular endothelial growth factor