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An Automated Differential Nuclear Staining Assay for Accurate Determination of Mitocan Cytotoxicity
Published on: May 12, 2020
Mitochondria: Inadvertent targets in chemotherapy-induced skeletal muscle toxicity and wasting?
James C Sorensen1,2, Beatrice D Cheregi1, Cara A Timpani1,2
1Centre for Chronic Disease, College of Health and Biomedicine, Victoria University, Melbourne, 8001, Australia.
Abstract:
Chemotherapy has been associated with increased mitochondrial reactive oxygen species production, mitochondrial dysfunction and skeletal muscle atrophy leading to severe patient clinical complications including skeletal muscle fatigue, insulin resistance and wasting. The exact mechanisms behind this skeletal muscle toxicity are largely unknown, and as such co-therapies to attenuate chemotherapy-induced side effects are lacking. Here, we review the current literature describing the clinical manifestations and molecular origins of chemotherapy-induced myopathy with a focus on the mitochondria as the target organelle via which chemotherapeutic agents establish toxicity. We explore the likely mechanisms through which myopathy is induced, using the anthracycline doxorubicin, and the platinum-based alkylating agent oxaliplatin, as examples. Finally, we recommend directions for future research and outline the potential significance of these proposed directions.
Insights
Chemotherapy can cause skeletal muscle problems by damaging mitochondria, leading to fatigue and wasting. Understanding these mechanisms is key to developing treatments for chemotherapy-induced myopathy.
Area of Science:
- Biochemistry
- Cell Biology
- Oncology
Background:
- Chemotherapy often causes skeletal muscle atrophy and dysfunction.
- Mitochondrial damage is implicated in chemotherapy-induced skeletal muscle toxicity.
- Mechanisms of chemotherapy-induced myopathy are not fully understood, limiting co-therapy development.
Purpose of the Study:
- To review clinical and molecular aspects of chemotherapy-induced myopathy.
- To focus on mitochondria as the primary target of chemotherapy-induced muscle toxicity.
- To explore mechanisms using doxorubicin and oxaliplatin as examples.
Main Methods:
- Literature review of current research on chemotherapy-induced myopathy.
- Analysis of molecular pathways involving mitochondrial dysfunction.
- Examination of specific chemotherapeutic agents (doxorubicin, oxaliplatin).
Main Results:
- Chemotherapy increases mitochondrial reactive oxygen species (ROS) production.
- Mitochondrial dysfunction contributes to skeletal muscle atrophy, fatigue, and insulin resistance.
- Doxorubicin and oxaliplatin exemplify mechanisms of chemotherapy-induced myopathy.
Conclusions:
- Mitochondria are a critical target for chemotherapy-induced skeletal muscle toxicity.
- Further research into these mechanisms is needed to develop effective co-therapies.
- Understanding mitochondrial pathways can guide future therapeutic strategies against myopathy.
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