Conditional knockout of prolyl hydroxylase domain protein 2 attenuates high fat-diet-induced @entity299 in XXXX .

@entity32 @entity19 @entity26 @entity34925 @entity5001 @entity71957 @entity299 @entity8024 @entity637 @entity61361 @entity413
@entity26 sensor prolyl hydroxylases (PHDs) play important roles in the regulation of HIF-a and cell metabolisms. This study was designed to investigate the direct role of @entity34925 in high fat-diet (HFD)-induced @entity299 . In HFD fed @entity19 , @entity34925 expression was increased without significant changes in @entity71957 and @entity61361 levels in the heart. This was accompanied by a significant upregulation of @entity5001 ( @entity5001 ) and NF-kB. To explore the role of @entity34925 in HFD-induced @entity299 , @entity34925 conditional knockout @entity19 were fed a HFD for 16 weeks. Intriguingly, knockout of @entity34925 significantly reduced @entity5001 and NF-kb expression in HFD @entity19 hearts. Moreover, knockout of @entity34925 inhibited @entity637 and @entity8024 expression, and reduced cell apoptosis and macrophage infiltration in HFD @entity19 . This was accompanied by a significant improvement of cardiac function. Most importantly, conditional knockout of @entity34925 at late stage in HFD @entity19 significantly improved @entity413 tolerance and reversed @entity299 . Our studies demonstrate that @entity34925 activity is a critical contributor to the HFD-induced @entity299 . Inhibition of @entity34925 attenuates HFD-induced @entity299 by a mechanism involving suppression of @entity5001 /NF-kb pathway and @entity32 .
