Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediated
Myocardial infarction is the leading cause of death and disability worldwide, and the development of new treatments can help reduce the size of myocardial infarction and prevent adverse cardiovascular events. Cardiac repair after myocardial infarction can effectively remove necrotic tissue, induce n...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2023-01-01
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| Series: | Frontiers in Cardiovascular Medicine |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fcvm.2022.1077290/full |
| _version_ | 1797957685654585344 |
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| author | Tingting Li Zhipeng Yan Yajie Fan Xinbiao Fan Aolin Li Zhongwen Qi Junping Zhang |
| author_facet | Tingting Li Zhipeng Yan Yajie Fan Xinbiao Fan Aolin Li Zhongwen Qi Junping Zhang |
| author_sort | Tingting Li |
| collection | DOAJ |
| description | Myocardial infarction is the leading cause of death and disability worldwide, and the development of new treatments can help reduce the size of myocardial infarction and prevent adverse cardiovascular events. Cardiac repair after myocardial infarction can effectively remove necrotic tissue, induce neovascularization, and ultimately replace granulation tissue. Cardiac inflammation is the primary determinant of whether beneficial cardiac repair occurs after myocardial infarction. Immune cells mediate inflammatory responses and play a dual role in injury and protection during cardiac repair. After myocardial infarction, genetic ablation or blocking of anti-inflammatory pathways is often harmful. However, enhancing endogenous anti-inflammatory pathways or blocking endogenous pro-inflammatory pathways may improve cardiac repair after myocardial infarction. A deficiency of neutrophils or monocytes does not improve overall cardiac function after myocardial infarction but worsens it and aggravates cardiac fibrosis. Several factors are critical in regulating inflammatory genes and immune cells’ phenotypes, including DNA methylation, histone modifications, and non-coding RNAs. Therefore, strict control and timely suppression of the inflammatory response, finding a balance between inflammatory cells, preventing excessive tissue degradation, and avoiding infarct expansion can effectively reduce the occurrence of adverse cardiovascular events after myocardial infarction. This article reviews the involvement of neutrophils, monocytes, macrophages, and regulatory T cells in cardiac repair after myocardial infarction. After myocardial infarction, neutrophils are the first to be recruited to the damaged site to engulf necrotic cell debris and secrete chemokines that enhance monocyte recruitment. Monocytes then infiltrate the infarct site and differentiate into macrophages and they release proteases and cytokines that are harmful to surviving myocardial cells in the pre-infarct period. As time progresses, apoptotic neutrophils are cleared, the recruitment of anti-inflammatory monocyte subsets, the polarization of macrophages toward the repair phenotype, and infiltration of regulatory T cells, which secrete anti-inflammatory factors that stimulate angiogenesis and granulation tissue formation for cardiac repair. We also explored how epigenetic modifications regulate the phenotype of inflammatory genes and immune cells to promote cardiac repair after myocardial infarction. This paper also elucidates the roles of alarmin S100A8/A9, secreted frizzled-related protein 1, and podoplanin in the inflammatory response and cardiac repair after myocardial infarction. |
| first_indexed | 2024-04-11T00:07:39Z |
| format | Article |
| id | doaj.art-62ab859ec1984b7ea6d2f065b1f7ec7f |
| institution | Directory Open Access Journal |
| issn | 2297-055X |
| language | English |
| last_indexed | 2024-04-11T00:07:39Z |
| publishDate | 2023-01-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cardiovascular Medicine |
| spelling | doaj.art-62ab859ec1984b7ea6d2f065b1f7ec7f2023-01-09T09:36:05ZengFrontiers Media S.A.Frontiers in Cardiovascular Medicine2297-055X2023-01-01910.3389/fcvm.2022.10772901077290Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediatedTingting Li0Zhipeng Yan1Yajie Fan2Xinbiao Fan3Aolin Li4Zhongwen Qi5Junping Zhang6First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin, ChinaGraduate School, Tianjin University of Traditional Chinese Medicine, Tianjin, ChinaGraduate School, Tianjin University of Traditional Chinese Medicine, Tianjin, ChinaGraduate School, Tianjin University of Traditional Chinese Medicine, Tianjin, ChinaGraduate School, Tianjin University of Traditional Chinese Medicine, Tianjin, ChinaXiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing, ChinaFirst Teaching Hospital of Tianjin University of Traditional Chinese Medicine, National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, Tianjin, ChinaMyocardial infarction is the leading cause of death and disability worldwide, and the development of new treatments can help reduce the size of myocardial infarction and prevent adverse cardiovascular events. Cardiac repair after myocardial infarction can effectively remove necrotic tissue, induce neovascularization, and ultimately replace granulation tissue. Cardiac inflammation is the primary determinant of whether beneficial cardiac repair occurs after myocardial infarction. Immune cells mediate inflammatory responses and play a dual role in injury and protection during cardiac repair. After myocardial infarction, genetic ablation or blocking of anti-inflammatory pathways is often harmful. However, enhancing endogenous anti-inflammatory pathways or blocking endogenous pro-inflammatory pathways may improve cardiac repair after myocardial infarction. A deficiency of neutrophils or monocytes does not improve overall cardiac function after myocardial infarction but worsens it and aggravates cardiac fibrosis. Several factors are critical in regulating inflammatory genes and immune cells’ phenotypes, including DNA methylation, histone modifications, and non-coding RNAs. Therefore, strict control and timely suppression of the inflammatory response, finding a balance between inflammatory cells, preventing excessive tissue degradation, and avoiding infarct expansion can effectively reduce the occurrence of adverse cardiovascular events after myocardial infarction. This article reviews the involvement of neutrophils, monocytes, macrophages, and regulatory T cells in cardiac repair after myocardial infarction. After myocardial infarction, neutrophils are the first to be recruited to the damaged site to engulf necrotic cell debris and secrete chemokines that enhance monocyte recruitment. Monocytes then infiltrate the infarct site and differentiate into macrophages and they release proteases and cytokines that are harmful to surviving myocardial cells in the pre-infarct period. As time progresses, apoptotic neutrophils are cleared, the recruitment of anti-inflammatory monocyte subsets, the polarization of macrophages toward the repair phenotype, and infiltration of regulatory T cells, which secrete anti-inflammatory factors that stimulate angiogenesis and granulation tissue formation for cardiac repair. We also explored how epigenetic modifications regulate the phenotype of inflammatory genes and immune cells to promote cardiac repair after myocardial infarction. This paper also elucidates the roles of alarmin S100A8/A9, secreted frizzled-related protein 1, and podoplanin in the inflammatory response and cardiac repair after myocardial infarction.https://www.frontiersin.org/articles/10.3389/fcvm.2022.1077290/fullinflammationmyocardial infarctioncardiac repairinflammatory cellsepigenetic modificationstwo-way adjustment |
| spellingShingle | Tingting Li Zhipeng Yan Yajie Fan Xinbiao Fan Aolin Li Zhongwen Qi Junping Zhang Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediated Frontiers in Cardiovascular Medicine inflammation myocardial infarction cardiac repair inflammatory cells epigenetic modifications two-way adjustment |
| title | Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediated |
| title_full | Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediated |
| title_fullStr | Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediated |
| title_full_unstemmed | Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediated |
| title_short | Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediated |
| title_sort | cardiac repair after myocardial infarction a two sided role of inflammation mediated |
| topic | inflammation myocardial infarction cardiac repair inflammatory cells epigenetic modifications two-way adjustment |
| url | https://www.frontiersin.org/articles/10.3389/fcvm.2022.1077290/full |
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