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Mitochondrial Dysfunction in Cardiac Disease: The Fort Fell

Overview
Journal Biomolecules
Publisher MDPI
Date 2025 Jan 8
PMID 39766241
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Abstract

Myocardial cells and the extracellular matrix achieve their functions through the availability of energy. In fact, the mechanical and electrical properties of the heart are heavily dependent on the balance between energy production and consumption. The energy produced is utilized in various forms, including kinetic, dynamic, and thermal energy. Although total energy remains nearly constant, the contribution of each form changes over time. Thermal energy increases, while dynamic and kinetic energy decrease, ultimately becoming insufficient to adequately support cardiac function. As a result, toxic byproducts, unfolded or misfolded proteins, free radicals, and other harmful substances accumulate within the myocardium. This leads to the failure of crucial processes such as myocardial contraction-relaxation coupling, ion exchange, cell growth, and regulation of apoptosis and necrosis. Consequently, both the micro- and macro-architecture of the heart are altered. Energy production and consumption depend on the heart's metabolic resources and the functional state of the cardiac structure, including cardiomyocytes, non-cardiomyocyte cells, and their metabolic and energetic behavior. Mitochondria, which are intracellular organelles that produce more than 95% of ATP, play a critical role in fulfilling all these requirements. Therefore, it is essential to gain a deeper understanding of their anatomy, function, and homeostatic properties.

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References
1.
Cheng M, Wang C, Shiao M, Liu M, Huang Y, Huang C . Metabolic disturbances identified in plasma are associated with outcomes in patients with heart failure: diagnostic and prognostic value of metabolomics. J Am Coll Cardiol. 2015; 65(15):1509-20. DOI: 10.1016/j.jacc.2015.02.018. View

2.
Grings M, Seminotti B, Karunanidhi A, Ghaloul-Gonzalez L, Mohsen A, Wipf P . ETHE1 and MOCS1 deficiencies: Disruption of mitochondrial bioenergetics, dynamics, redox homeostasis and endoplasmic reticulum-mitochondria crosstalk in patient fibroblasts. Sci Rep. 2019; 9(1):12651. PMC: 6718683. DOI: 10.1038/s41598-019-49014-2. View

3.
Lopez-Crisosto C, Pennanen C, Vasquez-Trincado C, Morales P, Bravo-Sagua R, Quest A . Sarcoplasmic reticulum-mitochondria communication in cardiovascular pathophysiology. Nat Rev Cardiol. 2017; 14(6):342-360. DOI: 10.1038/nrcardio.2017.23. View

4.
Rocha A, Franco A, Krezel A, Rumsey J, Alberti J, Knight W . MFN2 agonists reverse mitochondrial defects in preclinical models of Charcot-Marie-Tooth disease type 2A. Science. 2018; 360(6386):336-341. PMC: 6109362. DOI: 10.1126/science.aao1785. View

5.
Paolicelli R, Bergamini G, Rajendran L . Cell-to-cell Communication by Extracellular Vesicles: Focus on Microglia. Neuroscience. 2018; 405:148-157. DOI: 10.1016/j.neuroscience.2018.04.003. View