Mitochondrial Determinants of Anti-Cancer Drug-Induced Cardiotoxicity

Mitochondria are key organelles for the maintenance of myocardial tissue homeostasis, playing a pivotal role in adenosine triphosphate (ATP) production, calcium signaling, redox homeostasis, and thermogenesis, as well as in the regulation of crucial pathways involved in cell survival. On this basis,...

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Published in:Biomedicines 2022-02, Vol.10 (3), p.520
Main Authors: Rocca, Carmine, De Francesco, Ernestina Marianna, Pasqua, Teresa, Granieri, Maria Concetta, De Bartolo, Anna, Gallo Cantafio, Maria Eugenia, Muoio, Maria Grazia, Gentile, Massimo, Neri, Antonino, Angelone, Tommaso, Viglietto, Giuseppe, Amodio, Nicola
Format: Article
Language:English
Subjects:
Adenosine triphosphate
Anthracycline
anticancer therapy
Antitumor agents
Apoptosis
ATP
Calcium homeostasis
Calcium signalling
Cancer therapies
Cardiomyocytes
Cardiomyopathy
Cardiotoxicity
Cardiovascular diseases
Cell death
Cell survival
Chemotherapy
Congestive heart failure
Electron transport
Energy
Enzymes
Fatty acids
Gene expression
Heart failure
Homeostasis
Hydrogen peroxide
Ischemia
Kinases
Mitochondria
mitochondrial function
Muscle contraction
Organelles
Oxidation
Oxidative stress
Phosphorylation
Physiology
Proteasome inhibitors
Protein-tyrosine kinase receptors
Proteins
Quality control
Review
Structure-function relationships
Thermogenesis
Tumors
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Summary:Mitochondria are key organelles for the maintenance of myocardial tissue homeostasis, playing a pivotal role in adenosine triphosphate (ATP) production, calcium signaling, redox homeostasis, and thermogenesis, as well as in the regulation of crucial pathways involved in cell survival. On this basis, it is not surprising that structural and functional impairments of mitochondria can lead to contractile dysfunction, and have been widely implicated in the onset of diverse cardiovascular diseases, including ischemic cardiomyopathy, heart failure, and stroke. Several studies support mitochondrial targets as major determinants of the cardiotoxic effects triggered by an increasing number of chemotherapeutic agents used for both solid and hematological tumors. Mitochondrial toxicity induced by such anticancer therapeutics is due to different mechanisms, generally altering the mitochondrial respiratory chain, energy production, and mitochondrial dynamics, or inducing mitochondrial oxidative/nitrative stress, eventually culminating in cell death. The present review summarizes key mitochondrial processes mediating the cardiotoxic effects of anti-neoplastic drugs, with a specific focus on anthracyclines (ANTs), receptor tyrosine kinase inhibitors (RTKIs) and proteasome inhibitors (PIs).
ISSN:2227-9059
2227-9059
DOI:10.3390/biomedicines10030520