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Doxorubicin induces sarcoplasmic reticulum calcium regulation dysfunction via the decrease of SERCA2 and

Yachen Zhang1, Yu Chen, Min Zhang

  • 1Division of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kong Jiang Road, Shanghai, 200092, China, zhangyachen1965@126.com.

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Doxorubicin (DOX) treatment impairs cardiac sarcoplasmic reticulum (SR) calcium handling by reducing SERCA2 and phospholamban. This study reveals DOX-induced SR calcium regulation dysfunction in rats.

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Area of Science:

  • Cardiology
  • Pharmacology
  • Molecular Biology

Background:

  • Doxorubicin (DOX) is a widely used chemotherapy agent with known cardiotoxicity.
  • The precise mechanisms underlying DOX-induced cardiotoxicity, particularly concerning intracellular calcium regulation, require further elucidation.

Purpose of the Study:

  • To investigate the impact of doxorubicin (DOX) on calcium handling within the cardiac sarcoplasmic reticulum (SR).
  • To identify molecular changes in SR calcium regulatory proteins during DOX treatment.

Main Methods:

  • Sprague-Dawley rats received intravenous doxorubicin (DOX) at 1.5 mg/kg twice weekly for 12 treatments.
  • Evaluated hemodynamic parameters, myocardial oxidative stress markers, cardiac toxicity markers, and SR calcium handling capacity.
  • Assessed sarcoplasmic reticulum Ca(2+) absorption, Ca(2+)-stimulated ATPase activity, and levels of SERCA2 and phospholamban.

Main Results:

  • DOX treatment led to significant cardiac dysfunction, including decreased systolic and diastolic pressures and impaired contractility.
  • Increased markers of oxidative stress (iNOS, MDA, NO) and cardiac damage (AST, LDH, CPK, cTnI, BNP) were observed.
  • Crucially, DOX administration significantly reduced SR Ca(2+) uptake, Ca(2+)-stimulated ATPase activity, and the expression of SERCA2 and phospholamban.

Conclusions:

  • Doxorubicin (DOX) induces significant cardiac dysfunction and toxicity in rats.
  • DOX treatment leads to impaired sarcoplasmic reticulum (SR) calcium handling.
  • The observed SR calcium dysregulation is attributed to decreased expression of SERCA2 and phospholamban, highlighting a key mechanism of DOX cardiotoxicity.