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TLR2 and TLR3 expression as a biomarker for the risk of doxorubicin-induced heart failure

Shao Liang1, Cai Xinyong2, Zhu Hongmin2

  • 1Department of Cardiology, Jiangxi Provincial People's Hospital, No, 92 Aiguo Road, Donghu District, Nanchang, 330006, Jiangxi, People's Republic of China; Jiang Xi Provincial Institute of Cardiovascular Diseases, No, 92 Aiguo Road, Donghu District, Nanchang, 330006, Jiangxi, People's Republic of China.

Toxicology Letters
|July 1, 2018
PubMed

Insights

Toll-like receptors (TLRs) are implicated in doxorubicin-induced cardiotoxicity. This study found TLR2 and TLR3 expression changes in patients developing heart dysfunction after doxorubicin treatment, suggesting a predictive role for TLR2-TLR3 imbalance.

Area of Science:

  • Immunology
  • Cardiology
  • Pharmacology

Background:

  • Doxorubicin (Dox) treatment can cause irreversible heart dysfunction.
  • Innate immune factors, such as toll-like receptors (TLRs), are involved in doxorubicin-induced cardiotoxicity.

Purpose of the Study:

  • To investigate the role of TLRs in doxorubicin-induced heart failure (HF).
  • To assess TLR expression patterns in patients undergoing Dox treatment and developing HF.

Main Methods:

  • Peripheral blood mononuclear cells (PBMCs) from healthy controls, HF patients, Dox-treated patients, and Dox-treated HF patients were analyzed.
  • RT-PCR and Western blotting were used to measure TLR mRNA and protein expression.
  • ELISA was employed to detect inflammatory factors.

Main Results:

  • TLR2 expression was increased, while TLR3 expression was decreased in Dox-treated patients compared to controls, and further altered in the Dox-HF group.
  • Serum inflammatory factors were similar across HF, Dox, and Dox-HF groups.
  • A significant imbalance in TLR2 and TLR3 expression was observed in Dox-induced heart dysfunction.

Conclusions:

  • TLR2 and TLR3 exhibit altered expression patterns in doxorubicin-induced cardiotoxicity.
  • The observed TLR2-TLR3 imbalance may serve as a predictive biomarker for doxorubicin-induced heart failure.
Keywords:
CardiotoxicityDoxorubicinHeart failureInflammationToll-like receptor

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