Increased LDL electronegativity in chronic kidney disease disrupts XXXX homeostasis resulting in @entity299 .

@entity1 @entity9136 @entity19 @entity409 @entity740 @entity27773 @entity842 @entity460 @entity299 @entity35 @entity65 @entity1002
@entity740 ( @entity740 ), an independent risk factor for @entity65 , is associated with abnormal lipoprotein metabolism. We examined whether electronegative low-density lipoprotein (LDL) is mechanistically linked to @entity299 in @entity1 with early @entity740 . We compared echocardiographic parameters between @entity1 with stage 2 @entity740 (n = 88) and normal controls (n = 89) and found that impaired relaxation was more common in @entity740 @entity1 . Reduction in estimated glomerular filtration rate was an independent predictor of @entity1002 . We then examined cardiac function in a @entity35 model of early @entity740 induced by unilateral nephrectomy (UNx) by analyzing pressure-volume loop data. The time constant of isovolumic pressure decay was longer and the maximal velocity of pressure fall was slower in UNx @entity35 than in controls. When we investigated the mechanisms underlying @entity409 , we found that LDL from @entity740 @entity1 and UNx @entity35 was more electronegative than LDL from their respective controls and that LDL from UNx @entity35 induced intracellular @entity460 overload in H9c2 cardiomyocytes in vitro. Furthermore, chronic administration of electronegative LDL, which signals through @entity27773 ( @entity27773 ), induced @entity409 in wild-type but not @entity27773 (-/-) @entity19 . In in vitro and in vivo experiments, @entity299 was associated with increased @entity460 transient resulting from @entity842 (NO)-dependent nitrosylation of SERCA2a due to increases in inducible NO synthase expression and endothelial NO synthase uncoupling. In conclusion, LDL becomes more electronegative in early @entity740 . This change disrupts SERCA2a-regulated @entity460 homeostasis, which may be the mechanism underlying @entity9136 .
