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Correction: Exploring Predictive Risk Factors for Myocardial Injury in Children Treated with Anthracyclines: A Pilot Study.

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Targeting the Apelin-APJ Axis: A Promising Strategy to Mitigate Anthracycline-Induced Cardiotoxicity.

Varsha G Desai1

  • 1Department of Research and Development, Dr. Vishwanath Karad MIT World Peace University, Pune, Maharashtra, India. varsha.desai@mitwpu.edu.in.

Cardiovascular Toxicology
|April 17, 2026
PubMed
Summary

The apelin-APJ signaling axis shows promise for protecting the heart from anthracycline-induced cardiotoxicity. Targeting this pathway may offer a more effective cardioprotective strategy than current treatments.

Keywords:
AnthracyclinesApelin–APJ signalling axisCardioprotectionCardiotoxicityModified apelin analoguesNative apelin peptides

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Area of Science:

  • Cardiovascular Research
  • Pharmacology
  • Molecular Medicine

Background:

  • Anthracycline chemotherapy can cause long-term cardiotoxicity, leading to heart failure.
  • Current cardioprotective drugs have limited efficacy against the complex mechanisms of this toxicity.
  • Oxidative stress and mitochondrial dysfunction are key contributors to anthracycline-induced cardiotoxicity.

Purpose of the Study:

  • To review the potential of the apelin-APJ signaling axis as a novel therapeutic target for anthracycline-induced cardiotoxicity.
  • To highlight the cardioprotective mechanisms of apelin-APJ signaling.
  • To explore the therapeutic promise of apelin-APJ agonists in mitigating chemotherapy-related cardiac damage.

Main Methods:

  • Literature review of studies on apelin-APJ signaling in cardiovascular disease.
  • Analysis of preclinical and clinical data on apelin analogues.
  • Examination of signaling pathways implicated in anthracycline cardiotoxicity and their relation to apelin-APJ.

Main Results:

  • The apelin-APJ axis exerts beneficial effects including antioxidant, anti-apoptotic, and anti-inflammatory actions.
  • These effects are mediated via key pathways like PI3K/Akt and AMPK, which are impaired in cardiotoxicity.
  • Modified apelin analogues demonstrate enhanced stability and efficacy in cardiovascular models.

Conclusions:

  • Pharmacological activation of the apelin-APJ axis presents a promising, mechanism-based strategy against anthracycline cardiotoxicity.
  • Apelin-APJ agonists may offer superior cardioprotection compared to conventional therapies.
  • Further research into apelin-APJ targeted therapies is warranted for preventing chemotherapy-induced heart failure.