Dietary branched-chain amino acids get to the heart of H3K23Pr

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 t...

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Main Authors: Christina Demetriadou, Daniel S. Kantner, Nathaniel W. Snyder
Format: Article
Language:English
Published: American Society for Clinical Investigation 2023-11-01
Series:The Journal of Clinical Investigation
Online Access:https://doi.org/10.1172/JCI174953
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author Christina Demetriadou
Daniel S. Kantner
Nathaniel W. Snyder
author_facet Christina Demetriadou
Daniel S. Kantner
Nathaniel W. Snyder
author_sort Christina Demetriadou
collection DOAJ
description 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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spelling doaj.art-6289a5edb5a34c94a40a3cfa42848e472023-11-07T16:21:05ZengAmerican Society for Clinical InvestigationThe Journal of Clinical Investigation1558-82382023-11-0113322Dietary branched-chain amino acids get to the heart of H3K23PrChristina DemetriadouDaniel S. KantnerNathaniel W. SnyderCardiac 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.https://doi.org/10.1172/JCI174953
spellingShingle Christina Demetriadou
Daniel S. Kantner
Nathaniel W. Snyder
Dietary branched-chain amino acids get to the heart of H3K23Pr
The Journal of Clinical Investigation
title Dietary branched-chain amino acids get to the heart of H3K23Pr
title_full Dietary branched-chain amino acids get to the heart of H3K23Pr
title_fullStr Dietary branched-chain amino acids get to the heart of H3K23Pr
title_full_unstemmed Dietary branched-chain amino acids get to the heart of H3K23Pr
title_short Dietary branched-chain amino acids get to the heart of H3K23Pr
title_sort dietary branched chain amino acids get to the heart of h3k23pr
url https://doi.org/10.1172/JCI174953
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