AI Article Synopsis
- Cardiac metabolism not only powers the heart but also influences gene expression through signaling metabolites, which become dysfunctional in heart failure.
- Yang et al. report that a low-branched chain amino acid (BCAA) diet has protective benefits in a mouse model of heart failure.
- Their research highlights the role of a specific histone modification, influenced by the BCAA isoleucine, in managing the heart's stress response and suggests that dietary or pharmacological changes could help slow down heart enlargement.
Article Abstract
Cardiac metabolism provides effects that extend beyond the transformation of energy for the heart to operate effectively. Some metabolites also function as signaling molecules and exert transcriptional changes. Heart failure is a progressive pathology in which these metabolite functions falter. In this issue of the JCI, Yang et al. describe a protective effect from a low-branched chain amino acid (BCAA) diet in a mouse model of heart failure. The findings implicate a propionylation mark on histone H3 lysine 23 (H3K23Pr), previously shown to be dependent on the BCAA isoleucine, in transcriptional control of the cardiac stress response. The result underscores the interplay between metabolism and histone acylation, highlighting targeted dietary and pharmacological intervention as a means to decelerate cardiac hypertrophy.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10645384 | PMC |
| http://dx.doi.org/10.1172/JCI174953 | DOI Listing |
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