Mitochondria are Intracellular Organelles Characterized : A Part from the Book Chapter : Regulatory Mechanisms of Mitochondrial Volume in the Heart in Response to Physiological and Pathological Stimuli

Mitochondria are intracellular organelles characterized by a double-membrane structure: the inner mitochondrial membrane (IMM) and the outer mitochondrial membrane (OMM), separated by the intermembrane space (IMS). These organelles are pivotal for producing approximately 90% of cellular ATP in most eukaryotic cells. Beyond ATP synthesis, mitochondria are essential for maintaining cellular ion homeostasis and redox balance, participating in lipid metabolism, generating protein and DNA precursors, and producing reactive oxygen species (ROS). Mitochondria are particularly crucial in the heart, which requires substantial energy to maintain myofibrillar contractility and cellular ion homeostasis. For these reasons, various mechanisms operate to control cardiac oxidative and energy stress. Cardiac muscle cells (cardiomyocytes) are densely packed with mitochondria, constituting nearly 30% of the cell volume. The mitochondria are categorized based on their subcellular localization into intermyofibrillar, subsarcolemmal, and perinuclear mitochondria. This strategic distribution enables mitochondria to efficiently supply ATP to myofibrils and regulate Ca2+ flux, ROS levels, and the NAD+/NADH ratio, thus linking redox balance with energy demand. Mitochondria also play a vital role in managing oxidative and energy stress in cardiac cells through various regulatory mechanisms. Additionally, mitochondria are involved in several cell death pathways, including apoptosis, necroptosis, pyroptosis, ferroptosis, and autophagy-induced cell death. These functions underscore the significance of mitochondria in both the survival and death of cardiomyocytes, highlighting their role in cardiac health and disease.

Author(s) Details:

Xavier R. Chapa-Dubocq
Department of Physiology, School of Medicine, University of Puerto Rico, San Juan, PR, USA.

Keishla M. Rodríguez-Graciani
Department of Physiology, School of Medicine, University of Puerto Rico, San Juan, PR, USA.

Joseph Capella Muniz
Department of Physiology, School of Medicine, University of Puerto Rico, San Juan, PR, USA.

Jason N. Bazil
Department of Physiology, Michigan State University, East Lansing, MI 48824-1046, USA.

Nelson Escobales
Department of Physiology, School of Medicine, University of Puerto Rico, San Juan, PR, USA.

Sabzali Javadov
Department of Physiology, School of Medicine, University of Puerto Rico, San Juan, PR, USA.

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Recent Global Research Developments in Heart Bioenergetics: Mitochondrial Fusion and Respiratory Activity

Matters of the Heart in Bioenergetics: Mitochondrial Fusion and Respiratory Activity

• Contrary to the proposed idea that fusion leads to high respiratory activity and fission results in low activity, experimental data showed that maximal ADP-dependent respiration rates are equally high in both isolated heart mitochondria and permeabilized cardiomyocytes.
• Interestingly, cardiac cells lack a mitochondrial reticulum (continuous fusion structure) and instead have individual, regularly arranged mitochondria. These mitochondria play a crucial role in cell metabolism, calcium cycling, and respiration regulation [1].

Mitochondrial Function in Cardiac Regeneration

• Neonates undergo a metabolic shift from anaerobic glycolysis to oxidative phosphorylation during cardiac regeneration.
• Mitochondria play a central role in meeting the heart’s high energy demands. A robust mitochondrial network is essential for cellular energy, cardiac health, and regenerative capacity [2].

Mitochondrial Dynamics and Cardiomyocyte Integrity

• Beyond ROS generation, mitochondrial dynamics (fusion and fission) are crucial for maintaining normal mitochondria number and morphology.
• Cardiomyocyte integrity relies on well-regulated mitochondrial dynamics[3] .

References

1. Varikmaa, M., Guzun, R., Grichine, A. et al. Matters of the heart in bioenergetics: mitochondrial fusion into continuous reticulum is not needed for maximal respiratory activity. J Bioenerg Biomembr 45, 319–331 (2013). https://doi.org/10.1007/s10863-012-9494-4
2. Chen, YX., Zhao, AR., Wei, TW. et al. Progress of Mitochondrial Function Regulation in Cardiac Regeneration. J. of Cardiovasc. Trans. Res. (2024). https://doi.org/10.1007/s12265-024-10514-w
3. Marín-García, J., Akhmedov, A.T. & Moe, G.W. Mitochondria in heart failure: the emerging role of mitochondrial dynamics. Heart Fail Rev 18, 439–456 (2013). https://doi.org/10.1007/s10741-012-9330-2

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