Key result
MicroRNAs modulate doxorubicin-induced cardiotoxicity by regulating the PI3K/Akt/p53 and Sirt1/Nrf2 signaling pathways, affecting cardiac apoptosis and oxidative stress.
Why the study?
Irreversible cardiotoxicity is the major limitation in the clinical use of DOX for solid tumors, involving microRNAs that exacerbate or suppress cardiac damage.
This review highlights the mechanistic role of microRNAs in regulating key signaling pathways involved in doxorubicin-induced cardiotoxicity, offering potential therapeutic targets.
Hypothesis-generating for microRNA interventions in doxorubicin cardiotoxicity; prospective trials needed before clinical adoption.
Doxorubicin (DOX) is used as a chemotherapeutic agent in the treatment of solid tumors. Irreversible cardiotoxicity is the major limitation in the clinical use of DOX. Several microRNAs (miRNAs) with diversified functions are identified that participate in exacerbating or suppressing DOX-induced cardiac damage. The miRNAs are small noncoding regulatory RNAs that modify the expression of the native genes. Studies have demonstrated that miRNAs by modifying the expression of proteins such as PTEN, Akt, and survivin can affect DOX-induced cardiac apoptosis. Moreover, miRNAs can modulate cardiac oxidative stress in DOX treatment through the posttranscriptional regulation of Sirt1, p66shc, and Nrf2 expressions. This manuscript has reviewed the regulation of the PI3K/Akt/p53 and the Sirt1/Nrf2 pathways by miRNAs in DOX-induced cardiotoxicity.
No takes yet. Share an insight, caveat, or question.
Yarmohammadi et al. (2022) conducted a review in Doxorubicin-induced cardiotoxicity. MicroRNAs was evaluated. MicroRNAs modulate doxorubicin-induced cardiotoxicity by regulating the PI3K/Akt/p53 and Sirt1/Nrf2 signaling pathways, affecting cardiac apoptosis and oxidative stress.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: