What is the clinical evidence from this study?

Study design: Systematic Review. Population: Doxorubicin-induced cardiotoxicity (n=24). Intervention: Transfection-based miRNA interventions (mimics and inhibitors). Primary outcome: Modulation of doxorubicin-induced cardiotoxicity.

What does this research mean for the field?

Transfection with specific microRNAs modulates doxorubicin-induced cardiotoxicity in preclinical models by attenuating or exacerbating oxidative stress, apoptosis, and non-apoptotic cell death pathways. Novelty: ClaimNovelty.SYNTHESIS. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To synthesize preclinical evidence on microRNAs functionally characterized through transfection-based approaches in models of doxorubicin-induced cardiotoxicity.

September 20, 2026European Journal of Pharmacology

Targeting MicroRNAs in Doxorubicin-Induced Cardiotoxicity: A Systematic Review of Transfection Studies

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Key result

Specific miRNA transfection modulates doxorubicin-induced cardiotoxicity in preclinical models by altering oxidative stress and apoptosis.

n=24

Population

24 preclinical studies (2015-2025) investigating doxorubicin-induced cardiotoxicity models

Design

Systematic_review

Authors

IDInderjit Singh Dhami SKSatinder KaurCentral University of Punjab GBGurjit Kaur BhattiChandigarh University

Discussion

Member takes

Overview

Highlights miRNAs as potential targets against doxorubicin cardiotoxicity; leaves open clinical translation from preclinical models.

Key Points

To synthesize preclinical evidence on microRNAs functionally characterized through transfection-based approaches in models of doxorubicin-induced cardiotoxicity.
Systematic review of 24 preclinical studies published between 2015 and 2025 evaluating microRNA mimics and inhibitors.
Included studies using downstream functional validation via quantitative reverse transcription PCR, Western blotting, and luciferase reporter assays.
Protective microRNAs (including miR-200a, miR-21, and miR-29b) reduced oxidative stress and cardiomyocyte apoptosis by activating the Keap1/Nrf2 pathway and suppressing Bax-dependent mitochondrial apoptosis.
Cardiotoxic microRNAs (including miR-140-5p, miR-128-3p, and miR-34a-5p) aggravated cardiac damage by suppressing antioxidant responses, impairing PPAR-γ and Sirt3 signaling, and promoting ferroptosis and pyroptosis.
Therapeutic progress remains restricted by a heavy reliance on non-human models, insufficient multi-pathway integration, and the lack of targeted in vivo delivery methods.

Study Design

Type

Systematic Review (n=24)

Structured PICO

Population

24 preclinical studies evaluating transfection-based miRNA interventions in doxorubicin-induced cardiotoxicity.

Intervention

Transfection-based approaches including miRNA mimics and inhibitors

Outcome

Modulation of doxorubicin-induced cardiotoxicity (including oxidative stress, apoptosis, ferroptotic, and pyroptotic cell death)surrogate

Specific microRNAs act as critical modulators of doxorubicin-induced cardiotoxicity, representing potential future pharmacological targets for cardioprotection.

Limitations

Predominance of non-human models
Limited pathway integration
Lack of clinically translatable delivery strategies
predominance of non-human models
limited pathway integration
lack of clinically translatable delivery strategies

Cite This Study

Dhami et al. (2026) conducted a systematic review in Doxorubicin-induced cardiotoxicity (n=24). Transfection-based miRNA interventions (mimics and inhibitors) was evaluated on Modulation of doxorubicin-induced cardiotoxicity. In a systematic review of 24 preclinical studies, transfection with specific miRNAs modulated doxorubicin-induced cardiotoxicity by attenuating or exacerbating oxidative stress and apoptosis.

synapsesocial.com/papers/6aaf9ae313be617d9320fefe https://doi.org/10.1016/j.ejphar.2026.179359

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September 20, 2026European Journal of Pharmacology

Targeting MicroRNAs in Doxorubicin-Induced Cardiotoxicity: A Systematic Review of Transfection Studies

View Full Paper

Ask AI

Bookmark

Key result

Specific miRNA transfection modulates doxorubicin-induced cardiotoxicity in preclinical models by altering oxidative stress and apoptosis.

n=24

Population

24 preclinical studies (2015-2025) investigating doxorubicin-induced cardiotoxicity models

Design

Systematic_review

Authors

IDInderjit Singh Dhami SKSatinder KaurCentral University of Punjab GBGurjit Kaur BhattiChandigarh University

Discussion

Member takes

Overview

Highlights miRNAs as potential targets against doxorubicin cardiotoxicity; leaves open clinical translation from preclinical models.

Key Points

To synthesize preclinical evidence on microRNAs functionally characterized through transfection-based approaches in models of doxorubicin-induced cardiotoxicity.
Systematic review of 24 preclinical studies published between 2015 and 2025 evaluating microRNA mimics and inhibitors.
Included studies using downstream functional validation via quantitative reverse transcription PCR, Western blotting, and luciferase reporter assays.
Protective microRNAs (including miR-200a, miR-21, and miR-29b) reduced oxidative stress and cardiomyocyte apoptosis by activating the Keap1/Nrf2 pathway and suppressing Bax-dependent mitochondrial apoptosis.
Cardiotoxic microRNAs (including miR-140-5p, miR-128-3p, and miR-34a-5p) aggravated cardiac damage by suppressing antioxidant responses, impairing PPAR-γ and Sirt3 signaling, and promoting ferroptosis and pyroptosis.
Therapeutic progress remains restricted by a heavy reliance on non-human models, insufficient multi-pathway integration, and the lack of targeted in vivo delivery methods.

Study Design

Type

Systematic Review (n=24)

Structured PICO

Population

24 preclinical studies evaluating transfection-based miRNA interventions in doxorubicin-induced cardiotoxicity.

Intervention

Transfection-based approaches including miRNA mimics and inhibitors

Outcome

Modulation of doxorubicin-induced cardiotoxicity (including oxidative stress, apoptosis, ferroptotic, and pyroptotic cell death)surrogate

Specific microRNAs act as critical modulators of doxorubicin-induced cardiotoxicity, representing potential future pharmacological targets for cardioprotection.

Limitations

Predominance of non-human models
Limited pathway integration
Lack of clinically translatable delivery strategies
predominance of non-human models
limited pathway integration
lack of clinically translatable delivery strategies

Cite This Study

synapsesocial.com/papers/6aaf9ae313be617d9320fefe https://doi.org/10.1016/j.ejphar.2026.179359

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