Autophagic therapeutic targeting for Doxorubicin-induced cardiomyopathy

Noha H Badr1, Eman G Khedr2

  • 1Department of Biochemistry, Faculty of Pharmacy, Tanta University, Tanta, 31527, Egypt. noha_hossam@pharm.tanta.edu.eg.

Insights

Doxorubicin (Dox) chemotherapy causes heart damage (cardiomyopathy) by altering autophagy, a cellular process. This review explores how modulating autophagy with drugs or natural products may protect the heart from Dox-induced cardiomyopathy.

Area of Science:

  • Cardiology
  • Oncology
  • Cell Biology

Background:

  • Doxorubicin (Dox) is a vital anticancer drug but causes cardiotoxicity, leading to Dox-induced cardiomyopathy (DIC).
  • The precise mechanisms by which Dox affects cellular autophagy in the heart remain unclear, with conflicting evidence on autophagy's role (cytoprotective vs. cytotoxic).

Purpose of the Study:

  • To review the therapeutic potential of modulating autophagy in Dox-induced cardiomyopathy.
  • To analyze how pharmacological drugs and natural products influence autophagic flux to mitigate cardiac damage.

Main Methods:

  • Literature review focusing on studies investigating autophagy modulation in Dox-induced cardiomyopathy.
  • Analysis of mechanistic roles of autophagy and therapeutic interventions targeting it.

Main Results:

  • Autophagy is significantly impacted by Dox administration, but its specific role in DIC is complex and debated.
  • Various interventions, including pharmacological agents and natural products, demonstrate potential in influencing autophagic flux to reduce cardiac damage.

Conclusions:

  • Modulating autophagy presents a promising therapeutic strategy for cardioprotection against Dox-induced cardiotoxicity.
  • Further research into the mechanistic role of autophagy in DIC is crucial for developing effective treatments.

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