ArticleJournal of cellular and molecular medicine2022
MicroRNA-495-3p diminishes doxorubicin-induced cardiotoxicity through activating AKT.
Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- miR-495-3p promotes chronic obstructive pulmonary disease by activating ferroptosis in lung epithelial cells through regulation of the ETS1/GPX4 axis.Molecular biology reports · 2026Article
- Circulating exosomal miRNA in acute coronary syndrome: mechanisms, clinical relevance and future directions.Frontiers in molecular biosciences · 2026Review
- A recent decade update on combating doxorubicin-induced toxicities.Archives of toxicology · 2025Review
- Deciphering the roles of cellular and extracellular non-coding RNAs in chemotherapy-induced cardiotoxicity.Molecular and cellular biochemistry · 2025Review
- LEF1 influences diabetic retinopathy and retinal pigment epithelial cell ferroptosisWorld journal of diabetes · 2025Article
- The role and mechanism of epigenetics in anticancer drug-induced cardiotoxicity.Basic research in cardiology · 2025Review
- Roles of Non-Coding RNA in Anthracycline Cardiotoxicity: A Narrative Review.Journal of inflammation research · 2025Review
- The Role of MicroRNAs in the Pathogenesis of Doxorubicin-Induced Vascular Remodeling.International journal of molecular sciences · 2024Review
- Circ-0006332 stimulates cardiomyocyte pyroptosis via the miR-143/TLR2 axis to promote doxorubicin-induced cardiac damage.Epigenetics · 2024Article
- Circulating MicroRNA as Biomarkers of Anthracycline-Induced Cardiotoxicity:JACC. CardioOncology · 2024Review
- Review
- Noncoding RNAs and Cardiac Fibrosis.Reviews in cardiovascular medicine · 2023Review
- MicroRNA-495-3p diminishes doxorubicin-induced cardiotoxicity through activating AKT.Journal of cellular and molecular medicine · 2022Article
- MicroRNAs in doxorubicin-induced cardiotoxicity: The DNA damage response.Frontiers in pharmacology · 2022Review
- Exosomes derived from mesenchymal stem cells ameliorate impaired glucose metabolism in myocardial Ischemia/reperfusion injury through miR-132-3p/PTEN/AKT pathway.Cell cycle (Georgetown, Tex.)Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Doxorubicin (Dox) is a broad-spectrum antitumour agent; however, its clinical application is impeded due to the cumulative cardiotoxicity. The present study aims to investigate the role and underlying mechanisms of microRNA-495-3p (miR-495-3p) in Dox-induced cardiotoxicity. Herein, we found that cardiac miR-495-3p expression was significantly decreased in Dox-treated hearts, and that the miR-495-3p agomir could prevent oxidative stress, cell apoptosis, cardiac mass loss, fibrosis and cardiac dysfunction upon Dox stimulation. In contrast, the miR-495-3p antagomir dramatically aggravated Dox-induced cardiotoxicity in mice. Besides, we found that the miR-495-3p agomir attenuated, while the miR-495-3p antagomir exacerbated Dox-induced oxidative stress and cellular injury in vitro. Mechanistically, we demonstrated that miR-495-3p directly bound to the 3'-untranslational region of phosphate and tension homology deleted on chromosome ten (PTEN), downregulated PTEN expression and subsequently activated protein kinase B (PKB/AKT) pathway, and that PTEN overexpression or AKT inhibition completely abolished the cardioprotective effects of the miR-495-3p agomir. Our study for the first time identify miR-495-3p as an endogenous protectant against Dox-induced cardiotoxicity through activating AKT pathway in vivo and in vitro.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.