Mitochondrial Determinants of Anti-Cancer Drug-Induced Cardiotoxicity
Key result
Anti-neoplastic drugs, including anthracyclines, RTKIs, and PIs, induce cardiotoxicity by altering the mitochondrial respiratory chain, energy production, and mitochondrial dynamics.
Why the study?
Mitochondrial targets are major determinants of the cardiotoxic effects triggered by chemotherapeutic agents, but the underlying mechanisms across different anticancer drug classes require summarization.
Design
Review
Authors
Discussion
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Member takes
Implication
Mitochondrial pathways may inform cardio-oncology monitoring; leaves open targeted interventions pending prospective trials.
Structured PICO
E
Exposure
Anti-neoplastic drugs (anthracyclines, receptor tyrosine kinase inhibitors, and proteasome inhibitors)
O
Outcome
Cardiotoxicity (mitochondrial structural and functional impairments)safety
This review highlights the central role of mitochondrial dysfunction in the cardiotoxic effects of major anti-cancer therapies, providing a mechanistic basis for cardio-oncology.
Cite This Study
Rocca et al. (2022) conducted a review in Anti-cancer drug-induced cardiotoxicity. Anti-neoplastic drugs (anthracyclines, RTKIs, and PIs) was evaluated. Anti-neoplastic drugs, including anthracyclines, RTKIs, and PIs, induce cardiotoxicity by altering the mitochondrial respiratory chain, energy production, and mitochondrial dynamics.