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Caloric excess or restriction mediated modulation of metabolic enzyme acetylation-proposed effects on cardiac growth
1Translational Medicine Branch, NHLBI, NIH, Bld 10-CRC, Room 5–3150, 10 Center Drive, Bethesda, MD, 20892-1454, USA. sackm@nhlbi.nih.gov
Abstract:
Caloric excess has been postulated to disrupt cardiac function via (i) the generation of toxic intermediates, (ii) via protein glycosylation and (iii) through the generation of reactive oxygen species. It is now increasingly being recognized that the nutrient intermediates themselves may modulate metabolic pathways through the post-translational modifications of metabolic enzymes. In light of the high energy demand of the heart, these nutrient mediated modulations in metabolic pathway functioning may play an important role in cardiac function and in the capacity of the heart to adapt to biomechanical stressors. In this review the role of protein acetylation and deacetylation in the control of metabolic programs is explored. Although not extensively investigated directly in the heart, the emerging data support that these nutrient mediated post-translational regulatory events (i) modulate cardiac metabolic pathways, (ii) integrate nutrient flux mediated post-translational effects with cardiac function and (iii) may be important in the development of cardiac pathology. Areas of investigation that need to be explored are highlighted. This article is part of a Special Issue entitled: Mitochondria and Cardioprotection.
Insights
Nutrient excess disrupts heart function. Protein acetylation and deacetylation regulate cardiac metabolism, impacting heart function and disease development.
Area of Science:
- Biochemistry
- Cardiology
- Metabolic Regulation
Background:
- Caloric excess can impair cardiac function through toxic intermediates, protein glycosylation, and reactive oxygen species.
- Nutrient intermediates can directly influence metabolic pathways via post-translational modifications of enzymes.
- The heart's high energy demand makes nutrient-mediated metabolic regulation crucial for cardiac function and stress adaptation.
Purpose of the Study:
- To review the role of protein acetylation and deacetylation in controlling cardiac metabolic programs.
- To explore how nutrient-mediated post-translational modifications impact cardiac metabolism and function.
- To identify key areas for future research in nutrient sensing and cardiac health.
Main Methods:
- Literature review focusing on protein acetylation/deacetylation in metabolic control.
- Analysis of emerging data on nutrient-mediated post-translational modifications in the heart.
- Synthesis of current understanding regarding cardiac metabolic pathways and adaptation.
Main Results:
- Emerging data suggest protein acetylation and deacetylation significantly modulate cardiac metabolic pathways.
- These regulatory events integrate nutrient flux with cardiac function and adaptation.
- Nutrient-mediated post-translational modifications are implicated in the development of cardiac pathology.
Conclusions:
- Protein acetylation and deacetylation are critical regulators of cardiac metabolism.
- These mechanisms link nutrient availability to cardiac function and disease.
- Further research is needed to fully elucidate these pathways in the heart.
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