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Mechanism of adipose-derived mesenchymal stem cell exosomes in the treatment of heart failure
BACKGROUND: Heart failure (HF) is a global health problem characterized by impaired heart function. Cardiac remodeling and cell death contribute to the development of HF. Although treatments such as digoxin and angiotensin receptor blocker drugs have been used, their effectiveness in reducing mortal...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Baishideng Publishing Group Inc
2023
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10600745/ https://www.ncbi.nlm.nih.gov/pubmed/37900939 http://dx.doi.org/10.4252/wjsc.v15.i9.897 |
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author | Wang, Lei Zhang, Jin-Jin Wang, Sha-Sha Li, Liang |
author_facet | Wang, Lei Zhang, Jin-Jin Wang, Sha-Sha Li, Liang |
author_sort | Wang, Lei |
collection | PubMed |
description | BACKGROUND: Heart failure (HF) is a global health problem characterized by impaired heart function. Cardiac remodeling and cell death contribute to the development of HF. Although treatments such as digoxin and angiotensin receptor blocker drugs have been used, their effectiveness in reducing mortality is uncertain. Researchers are exploring the use of adipose-derived mesenchymal stem cell (ADMSC) exosomes (Exos) as a potential therapy for HF. These vesicles, secreted by cells, may aid in tissue repair and regulation of inflammation and immune responses. However, further investigation is needed to understand the specific role of these vesicles in HF treatment. AIM: To investigate the mechanism of extracellular vesicles produced by ADMSC s in the treatment of HF. METHODS: Exogenous surface markers of ADMSCs were found, and ADMSCs were cultured. RESULTS: The identification of surface markers showed that the surface markers CD44 and CD29 of adipose-derived stem cells (ADSCs) were well expressed, while the surface markers CD45 and CD34 of ADSCs were negative, so the cultured cells were considered ADSCs. Western blotting detected the Exo surface marker protein, which expressed CD63 protein but did not express calnexin protein, indicating that ADSC-derived Exos were successfully extracted. CONCLUSION: The secretion of MSCs from adipose tissue can increase ATP levels, block cardiomyocyte apoptosis, and enhance the heart function of animals susceptible to HF. The inhibition of Bax, caspase-3 and p53 protein expression may be related to this process. |
format | Online Article Text |
id | pubmed-10600745 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Baishideng Publishing Group Inc |
record_format | MEDLINE/PubMed |
spelling | pubmed-106007452023-10-27 Mechanism of adipose-derived mesenchymal stem cell exosomes in the treatment of heart failure Wang, Lei Zhang, Jin-Jin Wang, Sha-Sha Li, Liang World J Stem Cells Basic Study BACKGROUND: Heart failure (HF) is a global health problem characterized by impaired heart function. Cardiac remodeling and cell death contribute to the development of HF. Although treatments such as digoxin and angiotensin receptor blocker drugs have been used, their effectiveness in reducing mortality is uncertain. Researchers are exploring the use of adipose-derived mesenchymal stem cell (ADMSC) exosomes (Exos) as a potential therapy for HF. These vesicles, secreted by cells, may aid in tissue repair and regulation of inflammation and immune responses. However, further investigation is needed to understand the specific role of these vesicles in HF treatment. AIM: To investigate the mechanism of extracellular vesicles produced by ADMSC s in the treatment of HF. METHODS: Exogenous surface markers of ADMSCs were found, and ADMSCs were cultured. RESULTS: The identification of surface markers showed that the surface markers CD44 and CD29 of adipose-derived stem cells (ADSCs) were well expressed, while the surface markers CD45 and CD34 of ADSCs were negative, so the cultured cells were considered ADSCs. Western blotting detected the Exo surface marker protein, which expressed CD63 protein but did not express calnexin protein, indicating that ADSC-derived Exos were successfully extracted. CONCLUSION: The secretion of MSCs from adipose tissue can increase ATP levels, block cardiomyocyte apoptosis, and enhance the heart function of animals susceptible to HF. The inhibition of Bax, caspase-3 and p53 protein expression may be related to this process. Baishideng Publishing Group Inc 2023-09-26 2023-09-26 /pmc/articles/PMC10600745/ /pubmed/37900939 http://dx.doi.org/10.4252/wjsc.v15.i9.897 Text en ©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved. https://creativecommons.org/licenses/by-nc/4.0/This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. |
spellingShingle | Basic Study Wang, Lei Zhang, Jin-Jin Wang, Sha-Sha Li, Liang Mechanism of adipose-derived mesenchymal stem cell exosomes in the treatment of heart failure |
title | Mechanism of adipose-derived mesenchymal stem cell exosomes in the treatment of heart failure |
title_full | Mechanism of adipose-derived mesenchymal stem cell exosomes in the treatment of heart failure |
title_fullStr | Mechanism of adipose-derived mesenchymal stem cell exosomes in the treatment of heart failure |
title_full_unstemmed | Mechanism of adipose-derived mesenchymal stem cell exosomes in the treatment of heart failure |
title_short | Mechanism of adipose-derived mesenchymal stem cell exosomes in the treatment of heart failure |
title_sort | mechanism of adipose-derived mesenchymal stem cell exosomes in the treatment of heart failure |
topic | Basic Study |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10600745/ https://www.ncbi.nlm.nih.gov/pubmed/37900939 http://dx.doi.org/10.4252/wjsc.v15.i9.897 |
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