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The Function of Mitochondrial Metabolism in Heart and Skeletal Muscle

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 20 October 2024 | Viewed by 1677

Special Issue Editor


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Guest Editor
Division of Cardiovascular Sciences, Department of Medicine, UC San Diego, La Jolla, CA 92093, USA
Interests: cardiovascular and skeletal muscle metabolic function

Special Issue Information

Dear Colleagues,

Mitochondria are often called the "powerhouses" of the cell because they play a critical role in producing the energy needed for cellular processes. This is particularly important in tissues with high energy demands, such as the heart and skeletal muscle.

In the heart, mitochondrial metabolism is essential for maintaining normal cardiac function. The heart relies heavily on oxidative metabolism to generate ATP, which is the primary energy source for cardiac muscle contraction. Mitochondrial dysfunction has been linked to numerous cardiac pathologies, including heart failure and arrhythmias. In addition to ATP production, mitochondria in the heart also play essential roles in calcium handling, reactive oxygen species (ROS) generation, and apoptosis.

Similarly, skeletal muscle also requires high levels of ATP to sustain muscle contraction during exercise. Mitochondria in skeletal muscle are critical for generating this ATP through oxidative phosphorylation. Additionally, mitochondrial metabolism in skeletal muscle is essential for regulating glucose and lipid metabolism, maintaining redox balance, contractile function, and regulating cell signaling pathways.

In both the heart and skeletal muscle, mitochondrial dysfunction can lead to impaired metabolism and energy production, contributing to the development of numerous pathologies, including heart failure and muscle dysfunction. Therefore, maintaining healthy mitochondrial function is crucial for the proper function of these tissues.

Papers related to any aspect of mitochondrial and energy metabolism in the heart and skeletal muscle and clinical reports will be considered for this Special Issue.

Dr. Yoshitake Cho
Guest Editor

Manuscript Submission Information

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Keywords

  • heart
  • skeletal muscle
  • metabolism
  • glucose
  • mitochondria
  • metabolic disorder

Published Papers (1 paper)

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Review

15 pages, 1236 KiB  
Review
Metabolic Flexibility of the Heart: The Role of Fatty Acid Metabolism in Health, Heart Failure, and Cardiometabolic Diseases
by Virginia Actis Dato, Stephan Lange and Yoshitake Cho
Int. J. Mol. Sci. 2024, 25(2), 1211; https://doi.org/10.3390/ijms25021211 - 19 Jan 2024
Cited by 1 | Viewed by 1334
Abstract
This comprehensive review explores the critical role of fatty acid (FA) metabolism in cardiac diseases, particularly heart failure (HF), and the implications for therapeutic strategies. The heart’s reliance on ATP, primarily sourced from mitochondrial oxidative metabolism, underscores the significance of metabolic flexibility, with [...] Read more.
This comprehensive review explores the critical role of fatty acid (FA) metabolism in cardiac diseases, particularly heart failure (HF), and the implications for therapeutic strategies. The heart’s reliance on ATP, primarily sourced from mitochondrial oxidative metabolism, underscores the significance of metabolic flexibility, with fatty acid oxidation (FAO) being a dominant source. In HF, metabolic shifts occur with an altered FA uptake and FAO, impacting mitochondrial function and contributing to disease progression. Conditions like obesity and diabetes also lead to metabolic disturbances, resulting in cardiomyopathy marked by an over-reliance on FAO, mitochondrial dysfunction, and lipotoxicity. Therapeutic approaches targeting FA metabolism in cardiac diseases have evolved, focusing on inhibiting or stimulating FAO to optimize cardiac energetics. Strategies include using CPT1A inhibitors, using PPARα agonists, and enhancing mitochondrial biogenesis and function. However, the effectiveness varies, reflecting the complexity of metabolic remodeling in HF. Hence, treatment strategies should be individualized, considering that cardiac energy metabolism is intricate and tightly regulated. The therapeutic aim is to optimize overall metabolic function, recognizing the pivotal role of FAs and the need for further research to develop effective therapies, with promising new approaches targeting mitochondrial oxidative metabolism and FAO that improve cardiac function. Full article
(This article belongs to the Special Issue The Function of Mitochondrial Metabolism in Heart and Skeletal Muscle)
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