Key result
Pulmonary artery banding induces shared right-heart proteomic shifts alongside distinct right atrial metabolic deficits.
Why the study?
Right heart failure involves both right atrial and right ventricular dysfunction, but the proteomic response of these distinct chambers to pressure overload remains undefined.
Proteomic analysis of right heart failure identifies shared metabolic alterations across both right chambers and distinct RA-specific deficits in the TCA cycle and BCAA metabolism, suggesting selective metabolic targets for right atrial dysfunction.
Animal model findings highlight right atrial metabolic pathways for mechanistic study in right heart failure; leaves open human translation and therapeutic relevance.
Right heart failure is due to both right atrial and right ventricular dysfunction. While the two chambers are distinct, the proteomic response to pressure overload is undefined. Here, we used quantitative proteomics to evaluate changes in both chambers in pulmonary artery banded pigs. We found common alterations in oxidative phosphorylation, ribosome regulation, integrin-mediated adhesion, and glycolysis enzymes. However, the right atrium had more pronounced deficits in the TCA cycle and branched-chain amino acid metabolism. Thus, these data highlight metabolic pathways that could be evaluated to selectively enhance right atrial function.
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Prins et al. (2026) studied Right heart failure (n=8). Pulmonary artery banding vs. Control pigs was evaluated on Differentially regulated proteins and enriched metabolic pathways in right atrium and right ventricle tissues. Pulmonary artery banding induced shared proteomic alterations in both right heart chambers alongside unique right atrial deficits in the TCA cycle and branched-chain amino acid metabolism.
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