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Published on: February 13, 2019
Cardiac metabolism in heart failure: implications beyond ATP production
Torsten Doenst1, Tien Dung Nguyen, E Dale Abel
1Department of Cardiothoracic Surgery, Jena University Hospital, Friedrich-Schiller-University Jena, Germany. doenst@med.uni-jena.de
Insights
Heart failure (HF) involves metabolic remodeling that impairs cardiac energetics and contractility. This remodeling also drives structural changes and oxidative stress, suggesting broader therapeutic targets beyond ATP production.
Area of Science:
- Cardiovascular Biology
- Metabolic Regulation
- Heart Failure Pathophysiology
Background:
- The heart requires substantial adenosine triphosphate (ATP) for continuous mechanical work.
- Cardiac metabolism alterations, termed metabolic remodeling, are observed in heart failure (HF).
- Metabolic remodeling in HF leads to ATP deficiency and impaired cardiac contractility.
Purpose of the Study:
- To emphasize that metabolic remodeling in HF has consequences beyond impaired energetics.
- To highlight the role of metabolic alterations in structural remodeling and oxidative stress during HF.
- To underscore the therapeutic potential of modulating cardiac metabolism in HF.
Main Methods:
- Characterization of cardiac metabolism in heart failure models.
- Analysis of metabolic remodeling, including substrate utilization and mitochondrial function.
- Investigation of the link between metabolic pathways and cellular processes like growth and regeneration.
Main Results:
- Metabolic remodeling in HF causes ATP deficiency and reduced contractility.
- Metabolic alterations contribute to structural remodeling and increased oxidative stress in the heart.
- Metabolic pathways provide building blocks and signaling molecules crucial for cellular functions.
Conclusions:
- Metabolic remodeling in HF impacts cardiac energetics, structural integrity, and oxidative balance.
- Therapeutic strategies targeting cardiac metabolism may offer benefits beyond improving energy supply.
- Understanding non-energetic consequences of metabolic remodeling is key for HF treatment.
Abstract:
The heart has a high rate of ATP production and turnover that is required to maintain its continuous mechanical work. Perturbations in ATP-generating processes may therefore affect contractile function directly. Characterizing cardiac metabolism in heart failure (HF) revealed several metabolic alterations called metabolic remodeling, ranging from changes in substrate use to mitochondrial dysfunction, ultimately resulting in ATP deficiency and impaired contractility. However, ATP depletion is not the only relevant consequence of metabolic remodeling during HF. By providing cellular building blocks and signaling molecules, metabolic pathways control essential processes such as cell growth and regeneration. Thus, alterations in cardiac metabolism may also affect the progression to HF by mechanisms beyond ATP supply. Our aim is therefore to highlight that metabolic remodeling in HF not only results in impaired cardiac energetics but also induces other processes implicated in the development of HF such as structural remodeling and oxidative stress. Accordingly, modulating cardiac metabolism in HF may have significant therapeutic relevance that goes beyond the energetic aspect.
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