Mitochondrial Ferritin in Subclinical Anthracycline-Induced Cardiotoxicity in Humans: A Pilot Study.

Doxorubicin-treated murine cardiomyocytes exhibited increased mitochondrial ferritin (MtFt) expression compared with untreated cells.

• MtFt expression was evaluated in primary murine cardiomyocytes before and after doxorubicin exposure.
• This in vitro finding served as the experimental basis for investigating MtFt as a potential biomarker in human patients.
• The study did not specify exact fold-change or quantitative values for MtFt upregulation in cardiomyocytes in the abstract.

A weak but significant inverse association was observed between MtFt levels and left ventricular ejection fraction (LVEF) at the end of treatment in cancer patients.

• The association was described as 'weak but significant', suggesting higher MtFt levels corresponded to lower LVEF values.
• LVEF was assessed at baseline, at the end of treatment, and 12 months after the first cycle.
• No patient in the cohort of 26 developed clinically relevant cardiotoxicity during the study period.
• The study was conducted in 26 cancer patients receiving anthracycline-based chemotherapy.

Multivariable linear regression showed no significant predictive effect of hsTnT, NT-proBNP, or time on MtFt changes.

• High-sensitivity troponin T (hsTnT) and N-terminal pro-brain natriuretic peptide (NT-proBNP) were assessed alongside MtFt at baseline, end of treatment, and 12 months after the first cycle.
• Neither established cardiac biomarker significantly predicted changes in MtFt levels in the multivariable model.
• Time as a variable also did not significantly predict MtFt changes in the regression model.

MtFt levels tended to decrease and hsTnT levels tended to increase over time in anthracycline-treated cancer patients.

• These trends were observed across three time points: baseline, end of treatment, and 12 months after the first cycle.
• The trends were described as tendencies rather than statistically significant findings in the multivariable analysis.
• The divergent trajectories of MtFt and hsTnT over time suggest potentially different biological mechanisms or temporal dynamics of these biomarkers.
• The sample size of 26 patients may have limited statistical power to detect significant longitudinal changes.

No patient in the 26-patient cohort developed clinically relevant cardiotoxicity during the study period.

• The study population consisted of 26 cancer patients monitored at baseline, end of treatment, and 12 months after the first anthracycline cycle.
• The absence of clinical cardiotoxicity means the study examined subclinical changes, consistent with the study's focus on subclinical anthracycline-induced cardiotoxicity.
• Monitoring included LVEF, hsTnT, and NT-proBNP as standard cardiotoxicity surveillance measures.

MtFt levels were assessed in peripheral blood cells of cancer patients as a non-invasive approach to monitoring anthracycline cardiotoxicity.

• Peripheral blood cells served as the biological sample for MtFt measurement, providing a clinically accessible biomarker source.
• Measurements were taken at three time points: baseline, end of treatment, and 12 months after the first cycle.
• This approach was designed to translate the murine cardiomyocyte findings into a human clinical context.
• The study is described as a pilot study, indicating preliminary and exploratory methodology.