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Myocardial Protection and Current Cancer Therapy: Two Opposite Targets with Inevitable Cost.

Panagiotis Efentakis1, Ioanna Andreadou1, Konstantinos E Iliodromitis2

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Cancer therapies targeting key cell signaling pathways can harm the heart, increasing risks of heart failure. This review examines VEGF, proteasome, and immune checkpoint inhibitors

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Area of Science:

  • Cardiology
  • Oncology
  • Pharmacology

Background:

  • Myocardial protection against ischemia/reperfusion injury (IRI) involves various signaling cascades.
  • Many signaling molecules crucial for cardioprotection are also implicated in cancer.
  • Anti-neoplastic drugs can weaken cardioprotective mechanisms and directly cause cardiotoxicity.

Purpose of the Study:

  • To review therapeutic interventions affecting myocardial cell signaling pathways.
  • To examine the opposing effects of VEGF, proteasome, and immune checkpoint inhibitors on intracellular cascades.
  • To discuss current guidelines for managing cancer therapy-induced cardiotoxicity.

Main Methods:

  • Narrative review of scientific literature.
  • Analysis of signaling pathways involved in myocardial protection and carcinogenesis.
  • Examination of cardiotoxicity induced by specific therapeutic interventions.

Main Results:

  • Anti-cancer drugs targeting common signaling pathways can compromise myocardial tolerance to stress.
  • VEGF, proteasome, and immune checkpoint inhibitors exert opposing effects on shared intracellular pathways.
  • Cardiotoxicity from cancer treatment can manifest as ventricular dysfunction or heart failure.

Conclusions:

  • Cancer therapies targeting cell signaling pathways pose a significant risk of cardiotoxicity.
  • Understanding the interplay between anti-cancer drugs and cardioprotective mechanisms is crucial.
  • Management of cardiotoxicity requires consideration of drug effects and cardiovascular confounders.