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Updated: Jun 26, 2025

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Transcriptomics coupled with proteomics reveals osimertinib-induced myocardial mitochondrial dysfunction.

Haichao Yang1, Suhua Qiu2, Tiezhu Yao1

  • 1Department of Cardiology, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050010, China.

Toxicology Letters
|May 11, 2024
PubMed
Summary

Osimertinib causes heart damage by disrupting mitochondrial function and reducing ATP production. This study reveals the mechanism behind this cardiotoxicity, offering insights for cancer patients undergoing treatment.

Keywords:
ATP synthaseCardiac toxicityMitochondrial dysfunctionOsimertinibOxidative phosphorylationTyrosine kinase inhibitor

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Area of Science:

  • Cardiology
  • Molecular Biology
  • Oncology

Background:

  • Osimertinib, an epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), is vital in cancer therapy.
  • Cardiac toxicity is a known side effect of osimertinib, but its underlying mechanisms remain unclear.

Purpose of the Study:

  • To elucidate the molecular mechanisms of osimertinib-induced cardiotoxicity.
  • To investigate the impact of osimertinib on cardiac mitochondrial function and energy production.

Main Methods:

  • Administered osimertinib to mice and neonatal rat ventricular myocytes (NRVMs).
  • Utilized 4D label-free proteomics and RNA-sequencing for comprehensive molecular profiling.
  • Performed Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis.

Main Results:

  • Osimertinib induced significant cardiac structural and functional damage in mice, with elevated injury biomarkers.
  • NRVMs treated with osimertinib showed enrichment of differentially expressed genes and proteins in oxidative phosphorylation (OXPHOs).
  • Osimertinib disrupted ATP synthase (complex V) function, leading to decreased adenosine triphosphate (ATP) levels and impaired mitochondrial function.

Conclusions:

  • Osimertinib-induced cardiotoxicity is mediated by mitochondrial dysfunction.
  • Disruption of OXPHOs and subsequent reduction in ATP production are key mechanisms driving cardiac damage.
  • Findings provide a mechanistic understanding of osimertinib cardiotoxicity, crucial for managing cancer patients.