# The mitigatory capabilities of exercise on breast cancer chemotherapy-induced cardiotoxicity

**Authors:** Chen-yue Qian, Juan Fan, Jing-yi Guo, Na Li, Xiang-qi Liu, Xiu Liu, Xiang-yuan Zeng, Cui-feng Huang, Cong Li, Hua-dong Liu, Jing-jin Liu

PMC · DOI: 10.3389/fcell.2025.1681702 · Frontiers in Cell and Developmental Biology · 2025-11-07

## TL;DR

This paper reviews how exercise can help reduce heart damage caused by breast cancer chemotherapy drugs.

## Contribution

The paper highlights the novel role of customized exercise regimens in mitigating chemotherapy-induced cardiotoxicity.

## Key findings

- Exercise regimens like aerobic training can reduce inflammation caused by chemotherapy drugs.
- Anthracyclines and HER2 blockers are major contributors to cardiotoxicity in breast cancer patients.
- Current cardiac rehabilitation programs lack focus on post-chemotherapy cardiotoxicity.

## Abstract

Chemotherapy drugs have significantly decreased breast cancer morbidity and mortality, but they have been associated with increased risk for adverse cardiovascular side effects, such as cardiotoxicity. These drugs generally fall under three broad categories: cell cycle inhibitors (ex. Anthracyclines, taxanes), human epidermal growth factor 2 (HER2) blockers (ex. Trastuzumab, pertuzumab), as well as other medications, such as the alkylating agent cyclophosphamide. This review analyzes the occurrence of specific cardiotoxic manifestations linked to increased heart failure risk, such as chest discomfort, edema, and dyspnea, as well as mechanisms of action, such as anthracycline inducing the generation of reactive oxygen species, for the aforementioned three drug categories. In particular, attention is given to anthracyclines and HER2 blockers, as they are two of the most commonly prescribed medications. On the other hand, the cardiotoxic effects of these medications have been found to be able to be mitigated by various exercise regimens, such as aerobic exercises, resistance training, and high intensity interval training. This review also examines the effectiveness of different regimens on alleviating post-chemotherapy cardiotoxicity in breast cancer patients, as well as the specific mechanisms involved, such as aerobic exercise being able to downregulate the expression of doxorubicin-induced pro-inflammatory factors (ex. Interleukin-8, cyclooxegenase-2, etc.). Moreover, the review points out the relative lack of cardiac rehabilitation programs specifically addressing the post-chemotherapeutic cardiotoxicity risks of breast cancer patients. Therefore, customized exercise regimens, accounting for breast cancer patient-specific medical profiles, should be developed to counteract against the adverse cardiovascular effects of chemotherapy.

## Linked entities

- **Chemicals:** doxorubicin (PubChem CID 31703), Interleukin-8 (PubChem CID 74974005)
- **Diseases:** breast cancer (MONDO:0004989), heart failure (MONDO:0005252)

## Full-text entities

- **Genes:** ERBB2 (erb-b2 receptor tyrosine kinase 2) [NCBI Gene 2064] {aka CD340, HER-2, HER-2/neu, HER2, MLN 19, MLN-19}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}
- **Diseases:** dyspnea (MESH:D004417), breast cancer (MESH:D001943), cardiotoxic (MESH:D066126), chest discomfort (MESH:D013898), inflammatory (MESH:D007249), edema (MESH:D004487), heart failure (MESH:D006333)
- **Chemicals:** doxorubicin (MESH:D004317), taxanes (MESH:D043823), Trastuzumab (MESH:D000068878), Anthracyclines (MESH:D018943), cyclophosphamide (MESH:D003520), reactive oxygen species (MESH:D017382), pertuzumab (MESH:C485206)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

171 references — full list in the complete paper: https://tomesphere.com/paper/PMC12634649/full.md

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Source: https://tomesphere.com/paper/PMC12634649