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June 9, 2021International Journal of Molecular SciencesOpen Access

Cinnamic acid derivatives protected rat and human cardiomyocytes against doxorubicin-induced cardiotoxicity by ameliorating oxidative stress, reducing caspase levels, and preventing motility inhibition.

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Why the study?

Clinical use of doxorubicin is severely limited by cumulative cardiotoxicity, and no universal and highly effective protective therapy has been introduced.

Population

Rat cardiomyocytes (H9c2) and human induced-pluripotent-stem-cell-derived cardiomyocytes (hiPSC-CMs)

Comparison

Cinnamic acid derivatives against doxorubicin-induced cardiotoxicity

Design

In vitro preclinical study

Key result

Cinnamic acid derivatives protected rat and human cardiomyocytes against doxorubicin-induced cardiotoxicity by ameliorating oxidative stress, reducing caspase levels, and preventing motility inhibition.

Authors

PKPaulina KoczurkiewiczKKKatarzyna KlaśAGAgnieszka Gunia‐Krzyżak

Discussion

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Overview

Does not support clinical use; leaves open further development of cinnamic acid derivatives against doxorubicin cardiotoxicity.

Structured PICO

P
Population
Rat cardiomyocytes (H9c2) and human induced-pluripotent-stem-cell-derived cardiomyocytes (hiPSC-CMs) exposed to doxorubicin
I
Intervention
Cinnamic acid (CA) derivatives
O
Outcome
Protection against doxorubicin-induced oxidative stress and viability reductionsurrogate

Cinnamic acid derivatives demonstrate multidirectional cardioprotective effects against doxorubicin-induced toxicity in vitro, suggesting potential as lead structures for novel cardioprotective therapeutics.

Cite This Study

Koczurkiewicz et al. (2021) studied Doxorubicin-induced cardiotoxicity. Cinnamic acid (CA) derivatives vs. Doxorubicin alone / control was evaluated on Oxidative stress, viability reduction, caspase-3 and -7 levels, motility inhibition, and cytoskeleton rearrangement. Cinnamic acid derivatives protected rat and human cardiomyocytes against doxorubicin-induced cardiotoxicity by ameliorating oxidative stress, reducing caspase levels, and preventing motility inhibition.

synapsesocial.com/papers/6a97240af69cd3f692022fa2https://doi.org/10.3390/ijms22126217
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Cinnamaldehyde alleviates doxorubicin-induced cardiotoxicity by decreasing oxidative stress and ferroptosis in cardiomyocytes2023 · 38 citations
  2. 2Calycosin ameliorates doxorubicin‐induced cardiotoxicity by suppressing oxidative stress and inflammation via the sirtuin 1–NOD‐like receptor protein 3 pathway2019 · 86 citations
  3. 3Carnosic acid protects against doxorubicin-induced cardiotoxicity through enhancing the Nrf2/HO-1 pathway2023 · 50 citations
  4. 4Effects of CAPE on biochemical, histopathological and cardiac parameters in doxorubicin induced cardiotoxicity2025 · 1 citations
  5. 5Molecular Insights into Doxorubicin-Induced Cardiotoxicity and Phytochemical-Based Cardioprotection: Challenges and Future Strategies2026 · 1 citations