Key result
Overexpression of miR-145-5p attenuated doxorubicin-induced cardiotoxicity, systolic dysfunction, and apoptosis by targeting SOX9 to inhibit NLRP3 inflammasome-mediated pyroptosis.
Why the study?
Doxorubicin causes dose-dependent cardiotoxicity limiting its utility, and although miR-145-5p shows cardioprotective properties in cardiovascular diseases, its role in doxorubicin-induced cardiomyopathy remains undefined.
Does miR-145-5p overexpression attenuate doxorubicin-induced heart injury in preclinical models?
Population
Wistar rats, H9C2 cells, and breast cancer patients before and after DOX treatment vs healthy controls
Comparison
AAV9-mediated miR-145-5p overexpression vs DOX controls
Design
Preclinical animal and cell study with clinical biomarker validation
Authors
Loading...
Preclinical protection against doxorubicin cardiotoxicity; leaves open clinical translation pending human studies.
Does miR-145-5p overexpression attenuate doxorubicin-induced heart injury in preclinical models?
miR-145-5p protects against doxorubicin-induced cardiotoxicity by targeting SOX9 to inhibit NLRP3 inflammasome-mediated pyroptosis, offering a potential therapeutic strategy.
Yu et al. (2025) studied Doxorubicin-induced cardiomyopathy. miR-145-5p overexpression via AAV9 vs. Doxorubicin treatment alone / controls was evaluated on Cardiotoxicity (systolic dysfunction, serum biomarkers, histopathological injury, apoptosis, oxidative stress, NLRP3 inflammasome activation). Overexpression of miR-145-5p attenuated doxorubicin-induced cardiotoxicity, systolic dysfunction, and apoptosis by targeting SOX9 to inhibit NLRP3 inflammasome-mediated pyroptosis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: