作者: Nathaniel Lal , Karanjit Puri , Brian Rodrigues
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摘要: In diabetes, compromised glucose utilization leads the heart to use FA almost exclusively for ATP generation. Chronically, this adaptation unfortunately conversion of potentially toxic metabolites. Paired with increased formation reactive oxygen species related excessive mitochondrial oxidation FA, can provoke cardiac cell death. To protect against demise, intrinsic mechanisms must be available heart. Vascular endothelial growth factor B (VEGFB) may one that plays an important role in protecting failure. As a member VEGF family, initial studies VEGFB focused on its angiogenesis. Surprisingly, does not appear play direct angiogenesis under normal conditions or even when overexpressed, but has been implicated influencing vascular indirectly by affecting VEGFA action. Intriguingly, also shown alter gene expression proteins involved metabolism and promote survival. Conversely, multiple models failure, including diabetic cardiomyopathy, have indicated significant drop VEGFB. review, we will discuss biology VEGFB, relationship cardiomyopathy.