Macrophages in organ fibrosis: from pathogenesis to therapeutic targets
Abstract Fibrosis, an excessive self-repair response, is an age-related pathological process that universally affects various major organs such as the heart, liver, kidney, and lungs. Continuous accumulation of pathological tissue fibrosis destroys structural integrity and causes loss of function, w...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Nature Publishing Group
2024-12-01
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| Series: | Cell Death Discovery |
| Online Access: | https://doi.org/10.1038/s41420-024-02247-1 |
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| _version_ | 1846137311825231872 |
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| author | Yuanyuan Jiang Rong Cai Yu Huang Like Zhu Long Xiao Caihong Wang Lihong Wang |
| author_facet | Yuanyuan Jiang Rong Cai Yu Huang Like Zhu Long Xiao Caihong Wang Lihong Wang |
| author_sort | Yuanyuan Jiang |
| collection | DOAJ |
| description | Abstract Fibrosis, an excessive self-repair response, is an age-related pathological process that universally affects various major organs such as the heart, liver, kidney, and lungs. Continuous accumulation of pathological tissue fibrosis destroys structural integrity and causes loss of function, with consequent organ failure and increased mortality. Although some differences exist in the triggering mechanisms and pathophysiologic manifestations of organ-specific fibrosis, they usually share similar cascading responses and features, including chronic inflammatory stimulation, parenchymal cell injury, and macrophage recruitment. Macrophages, due to their high plasticity, can polarize into different phenotypes in response to varied microenvironments and play a crucial role in the development of organ fibrosis. This review examined the relationship between macrophages and the pathogenesis of organ fibrosis. Moreover, it analyzed how fibrosis can be modulated by targeting macrophages, which may become a novel and promising therapeutic strategy for fibrosis. |
| format | Article |
| id | doaj-art-dbec73b12b4c4780b18a400e94872211 |
| institution | Kabale University |
| issn | 2058-7716 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | Nature Publishing Group |
| record_format | Article |
| series | Cell Death Discovery |
| spelling | doaj-art-dbec73b12b4c4780b18a400e948722112024-12-08T12:18:38ZengNature Publishing GroupCell Death Discovery2058-77162024-12-0110111110.1038/s41420-024-02247-1Macrophages in organ fibrosis: from pathogenesis to therapeutic targetsYuanyuan Jiang0Rong Cai1Yu Huang2Like Zhu3Long Xiao4Caihong Wang5Lihong Wang6Translational Medical Innovation Center, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese MedicineTranslational Medical Innovation Center, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese MedicineDepartment of Obstetrics and Gynecology, Zhangjiagang Hospital Affiliated to Soochow UniversityTranslational Medical Innovation Center, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese MedicineTranslational Medical Innovation Center, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese MedicineTranslational Medical Innovation Center, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese MedicineTranslational Medical Innovation Center, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese MedicineAbstract Fibrosis, an excessive self-repair response, is an age-related pathological process that universally affects various major organs such as the heart, liver, kidney, and lungs. Continuous accumulation of pathological tissue fibrosis destroys structural integrity and causes loss of function, with consequent organ failure and increased mortality. Although some differences exist in the triggering mechanisms and pathophysiologic manifestations of organ-specific fibrosis, they usually share similar cascading responses and features, including chronic inflammatory stimulation, parenchymal cell injury, and macrophage recruitment. Macrophages, due to their high plasticity, can polarize into different phenotypes in response to varied microenvironments and play a crucial role in the development of organ fibrosis. This review examined the relationship between macrophages and the pathogenesis of organ fibrosis. Moreover, it analyzed how fibrosis can be modulated by targeting macrophages, which may become a novel and promising therapeutic strategy for fibrosis.https://doi.org/10.1038/s41420-024-02247-1 |
| spellingShingle | Yuanyuan Jiang Rong Cai Yu Huang Like Zhu Long Xiao Caihong Wang Lihong Wang Macrophages in organ fibrosis: from pathogenesis to therapeutic targets Cell Death Discovery |
| title | Macrophages in organ fibrosis: from pathogenesis to therapeutic targets |
| title_full | Macrophages in organ fibrosis: from pathogenesis to therapeutic targets |
| title_fullStr | Macrophages in organ fibrosis: from pathogenesis to therapeutic targets |
| title_full_unstemmed | Macrophages in organ fibrosis: from pathogenesis to therapeutic targets |
| title_short | Macrophages in organ fibrosis: from pathogenesis to therapeutic targets |
| title_sort | macrophages in organ fibrosis from pathogenesis to therapeutic targets |
| url | https://doi.org/10.1038/s41420-024-02247-1 |
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