Comparative proteomic analysis of @entity35 left ventricle in a XXXX model.

@entity844 @entity296 @entity1369 @entity4123 @entity1283 @entity740 @entity3449 @entity7224 @entity512 @entity1154 @entity35 @entity815 @entity65 @entity2383
BACKGROUND: @entity740 ( @entity740 ) is associated with @entity1283 that leads to increased @entity65 and mortality. To date, use of the @entity3449 -angiotensin- @entity1369 system blockade has been the main treatment modality. However, @entity3449 -angiotensin- @entity1369 system blockade by the angiotensin converting enzyme inhibitors (ACEi) can only partially reverse the @entity1283 without having a significant impact on all-cause mortality as evidenced by meta-analyses from clinical trials. It is imperative to elucidate the molecular pathogenesis of @entity740 -related @entity296 for potential targets in further treatment. METHODS: Male @entity35 that underwent @entity512 (SNX) @entity35 were established as the @entity740 model. A hemodynamic study was used to evaluate the left ventricle (LV) structural and functional alterations. We used proteomic techniques to profile the LV protein changes among sham-operated @entity35 , SNX @entity35 , and SNX @entity35 with 6 months of ACEi enalapril interventions. The differentially expressed proteins were further annotated by functional and network analyses. RESULTS: As compared to the sham-operated @entity35 , the SNX @entity35 had 25 upregulated and 46 decreased protein expression. The top canonical pathways identified by ingenuity pathway analysis for the @entity740 were @entity2383 , oxidative phosphorylation, @entity844 b  oxidation, protein ubiquitination, and ketolysis. The most relevant functions extracted from these networks contained 27 and 23 focused proteins, respectively. They were related to cellular assembly and organization, RNA posttranscriptional modification, and protein synthesis. After ACEi  intervention for 6 weeks, the residual canonical pathways identified by ingenuity pathway analysis that mediated the @entity740 -related @entity296 were @entity2383 , ketolysis, @entity815 degradation IV, and @entity7224 degradation III. There were decreased @entity4123 and  SNRNP, and increased @entity1154 oxidase and SAHH expression in the LV of SNX @entity35 that could not be reversed by the ACEi. CONCLUSION: Our studies provide a repertoire of potential biomarkers related to @entity1283 in @entity740 . There are still residual disturbed molecules/pathways despite ACEi intervention. Further studies are warranted to investigate these potential novel targets to alleviate @entity740 -related @entity296 .
