Current Trends in Cardiology

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Short Communication - Current Trends in Cardiology (2023) Volume 7, Issue 10

Therapeutic strategies targeting cardiac metabolism to treat heart failure

Jingyi Hu*

Department of Cardiology, Shanghai Jiaotong University School of Medicine, Shanghai, China

*Corresponding Author:
Jingyi Hu
Department of Cardiology
Shanghai Jiaotong University School of Medicine
Shanghai, China

Received: 25-Sep-2023, Manuscript No. AACC-23-114269; Editor assigned: 27-Sep-2023, Pre QC No. AACC-23-114269(PQ); Reviewed: 12-Oct-2023, QC No. AACC-23-114269; Revised: 17-Oct-2023, Manuscript No. AACC-23-114269(R), Published: 24-Oct-2023,DOI:10.35841/aacc-7.10.206

Citation: Hu J. Therapeutic strategies targeting cardiac metabolism to treat heart failure. J Cell Biol Metab. 2023;7(10):206

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The heart is a remarkable organ with substantial energy requirements. It beats continuously throughout our lives, pumping blood to supply oxygen and nutrients to the body's tissues. To fuel this demanding job, the heart primarily relies on the conversion of various energy substrates into adenosine triphosphate (ATP), the cell's primary energy currency. The heart's ability to efficiently generate ATP is essential for its normal function.

In heart failure, the heart's ability to generate ATP becomes compromised. This metabolic dysfunction is a key contributor to the progression of the disease. There are several reasons behind the altered cardiac metabolism observed in heart failure.

Shift in Substrate Preference: In a healthy heart, fatty acids are the predominant energy source. However, in heart failure, the heart often shifts to using glucose as its primary substrate. This switch is less efficient and can lead to decreased ATP production [1].

Mitochondrial Dysfunction: Mitochondria are the powerhouse of the cell, responsible for ATP production. In heart failure, mitochondrial dysfunction occurs, reducing the heart's energygenerating capacity.

Reduced Oxygen Supply: The compromised blood supply to the heart muscle in heart failure limits the availability of oxygen, which is critical for efficient energy production through oxidative phosphorylation.

Altered Metabolite Levels: Heart failure is associated with changes in various metabolites, such as lactate, pyruvate, and citrate, which can further impair energy metabolism [2].

Given the pivotal role of cardiac metabolism in heart failure, therapeutic strategies aimed at restoring or enhancing metabolic function have gained significant attention. Here are some promising approaches:

Metabolic Modulators: Drugs that target specific metabolic pathways are being developed. For instance, drugs that promote fatty acid oxidation or enhance glucose utilization in the heart can help restore metabolic balance.

Mitochondrial Therapies: Strategies that focus on improving mitochondrial function are under investigation. These include mitochondrial-targeted antioxidants and compounds that support mitochondrial biogenesis.

Nutritional Interventions: Dietary modifications, such as ketogenic diets or supplements like coenzyme Q10, can potentially improve cardiac metabolism. These approaches aim to provide the heart with the necessary substrates for ATP production [3].

Gene Therapies: Advances in gene therapy offer the possibility of directly manipulating the genes responsible for cardiac metabolism. Researchers are exploring techniques to enhance the expression of genes involved in energy production. Exercise Training: Physical activity has a positive impact on cardiac metabolism. Exercise can promote mitochondrial health, improve substrate utilization, and enhance the heart's energy-producing capabilities.

Metabolite Profiling: Advanced techniques for metabolite profiling can help identify specific metabolic imbalances in heart failure patients. Personalized therapies can then be developed based on individual metabolic profiles.

Challenges and Future Directions

While the potential of targeting cardiac metabolism in heart failure is promising, several challenges remain:

Patient Heterogeneity: Heart failure is a heterogeneous condition, and metabolic dysfunction can vary between individuals. Tailoring therapies to specific patient profiles will be essential for optimal outcomes.

Safety Concerns: Manipulating metabolic pathways can have unintended consequences. Ensuring the safety of metabolictargeted therapies is crucial [4].

Combination Therapies: Heart failure is a multifaceted condition, and targeting metabolism alone may not be sufficient. Combination therapies that address various aspects of the disease will likely be needed.

Long-term Effects: The long-term effects of metabolic interventions need further study to assess their durability and impact on overall patient outcomes [5].


Therapeutic strategies targeting cardiac metabolism represent a promising avenue for treating heart failure. Restoring the heart's ability to generate ATP efficiently can potentially improve its function and alleviate the symptoms of heart failure. As research in this field continues to advance, it is hoped that these strategies will lead to more effective treatments for this challenging cardiovascular condition. However, translating these promising approaches into clinical practice requires rigorous testing and a comprehensive understanding of the complex metabolic processes at play in heart failure. With continued research and innovation, there is reason to be optimistic about the future of heart failure treatment.


  1. Inzucchi SE. How does empagliflozin reduce cardiovascular mortality? insights from a mediation analysis of the EMPA-REG OUTCOME trial. Diabetes Care. 2018;41:356-63.
  2. Indexed at, Google Scholar, Cross Ref

  3. Yurista SR. Sodium-glucose co-transporter 2 inhibition with empagliflozin improves cardiac function in non-diabetic rats with left ventricular dysfunction after myocardial infarction. Eur J Heart Fail. 2019;21:862-73.
  4. Indexed at, Google Scholar, Cross Ref

  5. Garg V. Mechanistic insights regarding the role of SGLT2 inhibitors and GLP1 agonist drugs on cardiovascular disease in diabetes. Prog Cardiovasc Dis. 2019;62:349-357.
  6. Indexed at, Google Scholar, Cross Ref

  7. McMurray JJV. DAPA-HF Trial Committees and Investigators . Dapagliflozin in patients with heart failure and reduced ejection fraction. N Engl J Med. 2019;381:1995-2008.
  8. Indexed at, Google Scholar, Cross Ref

  9. Hicks KA. Standardized Data Collection for Cardiovascular Trials Initiative (SCTI) . 2017 Cardiovascular and stroke endpoint definitions for clinical trials. J Am Coll Cardiol. 2018;71:1021-1034.
  10. Indexed at, Google Scholar, Cross Ref

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