ArticleCurrent medical science2025
Targeting miR-144-5p/ACSM1 Axis Alleviates Doxorubicin-Induced Heart Failure by Inhibiting Lipid Peroxidation.
Article in Current medical science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- The pathophysiological role of MiRNAs in heart failure.Frontiers in cardiovascular medicine · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study investigates the role of miR-144-5p in doxorubicin (DOX)-induced heart failure and explores its potential mechanisms by targeting ACSM1 and inhibiting lipid peroxidation.
methodsBioinformatics analysis was performed using the gene expression omnibus dataset GSE136547 to identify differentially expressed miRNAs in heart failure. DOX-induced in vitro and in vivo heart failure models were used to study the effects of miR-144-5p on cardiomyocyte viability, apoptosis, and lipid peroxidation. The targeting relationship between miR-144-5p and ACSM1 was verified using dual-luciferase reporter assays. Cardiac function was assessed by echocardiography, and biochemical markers of heart failure were measured using ELISA. The GO and KEGG enrichment analyses of ACSM1 were performed via the bioinformatic tools GeneMANIA and STRING.
resultsmiR-144-5p was significantly upregulated in DOX-treated cardiomyocytes and mouse hearts. Inhibition of miR-144-5p attenuated DOX-induced cardiomyocyte apoptosis, lipid peroxidation, and cardiac dysfunction. ACSM1 was identified as a direct target of miR-144-5p, and its expression was downregulated by DOX. Silencing ACSM1 abolished the protective effects of the miR-144-5p inhibitor on the viability, apoptosis, and lipid peroxidation of cardiomyocytes. Furthermore, miR-144-5p inhibition improved cardiac function in DOX-treated mice, as evidenced by reduced left ventricular dysfunction and decreased levels of heart failure markers (BNP, LDH, Ang II, and ALD).
conclusionsOur findings demonstrate that inhibiting miR-144-5p alleviates DOX-induced heart failure by targeting ACSM1 and suppressing lipid peroxidation. The miR-144-5p/ACSM1 axis may represent a novel therapeutic target for heart failure. Future studies should focus on further elucidating the mechanisms underlying this axis and exploring its potential clinical applications.
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Registered trials
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