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Targeting mitochondrial dynamics proteins for the treatment of doxorubicin-induced cardiotoxicity
Doxorubicin (DOX) is an extensively used chemotherapeutic agent that can cause severe and frequent cardiotoxicity, which limits its clinical application. Although there have been extensive researches on the cardiotoxicity caused by DOX, there is still a lack of effective treatment. It is necessary t...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10437218/ https://www.ncbi.nlm.nih.gov/pubmed/37602332 http://dx.doi.org/10.3389/fmolb.2023.1241225 |
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author | Chen, Rui Niu, Mengwen Hu, Xin He, Yuquan |
author_facet | Chen, Rui Niu, Mengwen Hu, Xin He, Yuquan |
author_sort | Chen, Rui |
collection | PubMed |
description | Doxorubicin (DOX) is an extensively used chemotherapeutic agent that can cause severe and frequent cardiotoxicity, which limits its clinical application. Although there have been extensive researches on the cardiotoxicity caused by DOX, there is still a lack of effective treatment. It is necessary to understand the molecular mechanism of DOX-induced cardiotoxicity and search for new therapeutic targets which do not sacrifice their anticancer effects. Mitochondria are considered to be the main target of cardiotoxicity caused by DOX. The imbalance of mitochondrial dynamics characterized by increased mitochondrial fission and inhibited mitochondrial fusion is often reported in DOX-induced cardiotoxicity, which can result in excessive ROS production, energy metabolism disorders, cell apoptosis, and various other problems. Also, mitochondrial dynamics disorder is related to tumorigenesis. Surprisingly, recent studies show that targeting mitochondrial dynamics proteins such as DRP1 and MFN2 can not only defend against DOX-induced cardiotoxicity but also enhance or not impair the anticancer effect. Herein, we summarize mitochondrial dynamics disorder in DOX-induced cardiac injury. Furthermore, we provide an overview of current pharmacological and non-pharmacological interventions targeting proteins involved in mitochondrial dynamics to alleviate cardiac damage caused by DOX. |
format | Online Article Text |
id | pubmed-10437218 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-104372182023-08-19 Targeting mitochondrial dynamics proteins for the treatment of doxorubicin-induced cardiotoxicity Chen, Rui Niu, Mengwen Hu, Xin He, Yuquan Front Mol Biosci Molecular Biosciences Doxorubicin (DOX) is an extensively used chemotherapeutic agent that can cause severe and frequent cardiotoxicity, which limits its clinical application. Although there have been extensive researches on the cardiotoxicity caused by DOX, there is still a lack of effective treatment. It is necessary to understand the molecular mechanism of DOX-induced cardiotoxicity and search for new therapeutic targets which do not sacrifice their anticancer effects. Mitochondria are considered to be the main target of cardiotoxicity caused by DOX. The imbalance of mitochondrial dynamics characterized by increased mitochondrial fission and inhibited mitochondrial fusion is often reported in DOX-induced cardiotoxicity, which can result in excessive ROS production, energy metabolism disorders, cell apoptosis, and various other problems. Also, mitochondrial dynamics disorder is related to tumorigenesis. Surprisingly, recent studies show that targeting mitochondrial dynamics proteins such as DRP1 and MFN2 can not only defend against DOX-induced cardiotoxicity but also enhance or not impair the anticancer effect. Herein, we summarize mitochondrial dynamics disorder in DOX-induced cardiac injury. Furthermore, we provide an overview of current pharmacological and non-pharmacological interventions targeting proteins involved in mitochondrial dynamics to alleviate cardiac damage caused by DOX. Frontiers Media S.A. 2023-08-03 /pmc/articles/PMC10437218/ /pubmed/37602332 http://dx.doi.org/10.3389/fmolb.2023.1241225 Text en Copyright © 2023 Chen, Niu, Hu and He. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Molecular Biosciences Chen, Rui Niu, Mengwen Hu, Xin He, Yuquan Targeting mitochondrial dynamics proteins for the treatment of doxorubicin-induced cardiotoxicity |
title | Targeting mitochondrial dynamics proteins for the treatment of doxorubicin-induced cardiotoxicity |
title_full | Targeting mitochondrial dynamics proteins for the treatment of doxorubicin-induced cardiotoxicity |
title_fullStr | Targeting mitochondrial dynamics proteins for the treatment of doxorubicin-induced cardiotoxicity |
title_full_unstemmed | Targeting mitochondrial dynamics proteins for the treatment of doxorubicin-induced cardiotoxicity |
title_short | Targeting mitochondrial dynamics proteins for the treatment of doxorubicin-induced cardiotoxicity |
title_sort | targeting mitochondrial dynamics proteins for the treatment of doxorubicin-induced cardiotoxicity |
topic | Molecular Biosciences |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10437218/ https://www.ncbi.nlm.nih.gov/pubmed/37602332 http://dx.doi.org/10.3389/fmolb.2023.1241225 |
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