Biomarkers of chemotherapy-induced cardiotoxicity: toward precision prevention using extracellular vesicles

Chemotherapy has revolutionized cancer treatment, offering hope to millions of patients worldwide. However, along with its benefits, chemotherapy can also bring about detrimental side effects, such as cardiotoxicity, which poses challenges in cancer management. Finding ways to prevent or mitigate these off-target effects is crucial for improving patient outcomes and enhancing the efficacy of cancer treatments.

In recent years, researchers have turned their attention to extracellular vesicles (EVs) as potential solutions to these challenges. EVs, tiny membrane-bound vesicles released by cells, are emerging as valuable biomarkers of health and disease, offering insights into molecular processes and cellular communication. Moreover, EVs hold promise as therapeutic agents to intervene at the cellular level, providing targeted treatments with fewer side effects.

Characteristics of EVs produced in response to different cellular death pathways

Shown is a schematic illustrating characteristics of EVs (cargo, surface proteins) released by cells undergoing several different forms of cellular death. DAMPS, damage-associated molecular patterns; HSP, heat shock proteins; LDH, lactate dehydrogenase; MLK, mixed lineage kinase; RER, rough endoplasmic reticulum.

One area where EVs show significant potential is in the context of chemotherapy-induced cardiotoxicity. Drugs like doxorubicin, while effective against cancer cells, can also harm healthy cardiac tissue, leading to serious complications. EVs, released in response to cellular stress and toxicity, may serve as early indicators of impending cardiotoxicity, offering clinicians a window of opportunity for intervention.

Additionally, EVs themselves may possess cardioprotective properties, shielding cardiac cells from the damaging effects of chemotherapy. By harnessing EVs as therapeutic agents, researchers aim to develop innovative strategies to prevent or offset chemotherapy-induced cardiotoxicity, improving patient safety and treatment outcomes.

However, the complexity of EVs presents challenges in their implementation as clinical tools. EV populations vary depending on the parent cells and cellular events, and the dynamic nature of cellular processes adds another layer of complexity. Understanding how EV cargo and signaling properties change under different conditions is essential for effectively harnessing EVs for cardioprotection.

Researchers from the National Institute of Environmental Health Sciences (NIEHS) highlight the potential of EVs as future clinical tools for mitigating chemotherapy-induced cardiotoxicity. By serving as both biomarkers and therapeutic agents, EVs offer a multifaceted approach to cardioprotection. However, further research is needed to unravel the complexities of EV signaling and to develop strategies for precise prevention of cardiotoxicity in anticancer treatments.

EVs represent a promising avenue for addressing the challenges of chemotherapy-induced cardiotoxicity. With continued research and innovation, EV-based therapies hold the potential to revolutionize cancer treatment by enhancing safety and efficacy, ultimately improving patient outcomes and quality of life.

Silver BB, Kreutz A, Weick M et al. (2024) Biomarkers of chemotherapy-induced cardiotoxicity: toward precision prevention using extracellular vesicles. Front Oncol [Epub ahead of print]. [article]

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