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The effect of immune cell‐derived exosomes in the cardiac tissue repair after myocardial infarction: Molecular mechanisms and pre‐clinical evidence
After a myocardial infarction (MI), the inflammatory responses are induced and assist to repair ischaemic injury and restore tissue integrity, but excessive inflammatory processes promote abnormal cardiac remodelling and progress towards heart failure. Thus, a timely resolution of inflammation and a...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8278122/ https://www.ncbi.nlm.nih.gov/pubmed/34092017 http://dx.doi.org/10.1111/jcmm.16686 |
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author | Wen, Heling Peng, Lei Chen, Yu |
author_facet | Wen, Heling Peng, Lei Chen, Yu |
author_sort | Wen, Heling |
collection | PubMed |
description | After a myocardial infarction (MI), the inflammatory responses are induced and assist to repair ischaemic injury and restore tissue integrity, but excessive inflammatory processes promote abnormal cardiac remodelling and progress towards heart failure. Thus, a timely resolution of inflammation and a firmly regulated balance between regulatory and inflammatory mechanisms can be helpful. Molecular‐ and cellular‐based approaches modulating immune response post‐MI have emerged as a promising therapeutic strategy. Exosomes are essential mediators of cell‐to‐cell communications, which are effective in modulating immune responses and immune cells following MI, improving the repair process of infarcted myocardium and maintaining ventricular function via the crosstalk among immune cells or between immune cells and myocardial cells. The present review aimed to seek the role of immune cell‐secreted exosomes in infarcted myocardium post‐MI, together with mechanisms behind their repairing impact on the damaged myocardium. The exosomes we focus on are secreted by classic immune cells including macrophages, dendritic cells, regulatory T cells and CD4(+) T cells; however, further research is demanded to determine the role of exosomes secreted by other immune cells, such as B cells, neutrophils and mast cells, in infarcted myocardium after MI. This knowledge can assist in the development of future therapeutic strategies, which may benefit MI patients. |
format | Online Article Text |
id | pubmed-8278122 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-82781222021-07-15 The effect of immune cell‐derived exosomes in the cardiac tissue repair after myocardial infarction: Molecular mechanisms and pre‐clinical evidence Wen, Heling Peng, Lei Chen, Yu J Cell Mol Med Reviews After a myocardial infarction (MI), the inflammatory responses are induced and assist to repair ischaemic injury and restore tissue integrity, but excessive inflammatory processes promote abnormal cardiac remodelling and progress towards heart failure. Thus, a timely resolution of inflammation and a firmly regulated balance between regulatory and inflammatory mechanisms can be helpful. Molecular‐ and cellular‐based approaches modulating immune response post‐MI have emerged as a promising therapeutic strategy. Exosomes are essential mediators of cell‐to‐cell communications, which are effective in modulating immune responses and immune cells following MI, improving the repair process of infarcted myocardium and maintaining ventricular function via the crosstalk among immune cells or between immune cells and myocardial cells. The present review aimed to seek the role of immune cell‐secreted exosomes in infarcted myocardium post‐MI, together with mechanisms behind their repairing impact on the damaged myocardium. The exosomes we focus on are secreted by classic immune cells including macrophages, dendritic cells, regulatory T cells and CD4(+) T cells; however, further research is demanded to determine the role of exosomes secreted by other immune cells, such as B cells, neutrophils and mast cells, in infarcted myocardium after MI. This knowledge can assist in the development of future therapeutic strategies, which may benefit MI patients. John Wiley and Sons Inc. 2021-06-05 2021-07 /pmc/articles/PMC8278122/ /pubmed/34092017 http://dx.doi.org/10.1111/jcmm.16686 Text en © 2021 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Reviews Wen, Heling Peng, Lei Chen, Yu The effect of immune cell‐derived exosomes in the cardiac tissue repair after myocardial infarction: Molecular mechanisms and pre‐clinical evidence |
title | The effect of immune cell‐derived exosomes in the cardiac tissue repair after myocardial infarction: Molecular mechanisms and pre‐clinical evidence |
title_full | The effect of immune cell‐derived exosomes in the cardiac tissue repair after myocardial infarction: Molecular mechanisms and pre‐clinical evidence |
title_fullStr | The effect of immune cell‐derived exosomes in the cardiac tissue repair after myocardial infarction: Molecular mechanisms and pre‐clinical evidence |
title_full_unstemmed | The effect of immune cell‐derived exosomes in the cardiac tissue repair after myocardial infarction: Molecular mechanisms and pre‐clinical evidence |
title_short | The effect of immune cell‐derived exosomes in the cardiac tissue repair after myocardial infarction: Molecular mechanisms and pre‐clinical evidence |
title_sort | effect of immune cell‐derived exosomes in the cardiac tissue repair after myocardial infarction: molecular mechanisms and pre‐clinical evidence |
topic | Reviews |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8278122/ https://www.ncbi.nlm.nih.gov/pubmed/34092017 http://dx.doi.org/10.1111/jcmm.16686 |
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