Injured Endothelial Cell: A Risk Factor for Pulmonary Fibrosis
The pathological features of pulmonary fibrosis (PF) are the abnormal activation and proliferation of myofibroblasts and the extraordinary deposition of the extracellular matrix (ECM). However, the pathogenesis of PF is still indistinct. In recent years, many researchers have realized that endotheli...
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-05-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/24/10/8749 |
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| author | Weiming Zhao Lan Wang Yaxuan Wang Hongmei Yuan Mengxia Zhao Hui Lian Shuaichen Ma Kai Xu Zhongzheng Li Guoying Yu |
| author_facet | Weiming Zhao Lan Wang Yaxuan Wang Hongmei Yuan Mengxia Zhao Hui Lian Shuaichen Ma Kai Xu Zhongzheng Li Guoying Yu |
| author_sort | Weiming Zhao |
| collection | DOAJ |
| description | The pathological features of pulmonary fibrosis (PF) are the abnormal activation and proliferation of myofibroblasts and the extraordinary deposition of the extracellular matrix (ECM). However, the pathogenesis of PF is still indistinct. In recent years, many researchers have realized that endothelial cells had a crucial role in the development of PF. Studies have demonstrated that about 16% of the fibroblasts in the lung tissue of fibrotic mice were derived from endothelial cells. Endothelial cells transdifferentiated into mesenchymal cells via the endothelial–mesenchymal transition (E(nd)MT), leading to the excessive proliferation of endothelial-derived mesenchymal cells and the accumulation of fibroblasts and ECM. This suggested that endothelial cells, a significant component of the vascular barrier, played an essential role in PF. Herein, this review discusses E(nd)MT and its contribution to the activation of other cells in PF, which could provide new ideas for further understanding the source and activation mechanism of fibroblasts and the pathogenesis of PF. |
| first_indexed | 2024-03-11T03:39:29Z |
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| id | doaj.art-5794d080d9d644028d02f868f1b95437 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-11T03:39:29Z |
| publishDate | 2023-05-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-5794d080d9d644028d02f868f1b954372023-11-18T01:41:11ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-05-012410874910.3390/ijms24108749Injured Endothelial Cell: A Risk Factor for Pulmonary FibrosisWeiming Zhao0Lan Wang1Yaxuan Wang2Hongmei Yuan3Mengxia Zhao4Hui Lian5Shuaichen Ma6Kai Xu7Zhongzheng Li8Guoying Yu9State Key Laboratory of Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang 453007, ChinaState Key Laboratory of Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang 453007, ChinaState Key Laboratory of Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang 453007, ChinaState Key Laboratory of Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang 453007, ChinaState Key Laboratory of Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang 453007, ChinaState Key Laboratory of Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang 453007, ChinaState Key Laboratory of Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang 453007, ChinaState Key Laboratory of Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang 453007, ChinaState Key Laboratory of Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang 453007, ChinaState Key Laboratory of Cell Differentiation and Regulation, Henan International Joint Laboratory of Pulmonary Fibrosis, Henan Center for Outstanding Overseas Scientists of Organ Fibrosis, Institute of Biomedical Science, College of Life Science, Henan Normal University, Xinxiang 453007, ChinaThe pathological features of pulmonary fibrosis (PF) are the abnormal activation and proliferation of myofibroblasts and the extraordinary deposition of the extracellular matrix (ECM). However, the pathogenesis of PF is still indistinct. In recent years, many researchers have realized that endothelial cells had a crucial role in the development of PF. Studies have demonstrated that about 16% of the fibroblasts in the lung tissue of fibrotic mice were derived from endothelial cells. Endothelial cells transdifferentiated into mesenchymal cells via the endothelial–mesenchymal transition (E(nd)MT), leading to the excessive proliferation of endothelial-derived mesenchymal cells and the accumulation of fibroblasts and ECM. This suggested that endothelial cells, a significant component of the vascular barrier, played an essential role in PF. Herein, this review discusses E(nd)MT and its contribution to the activation of other cells in PF, which could provide new ideas for further understanding the source and activation mechanism of fibroblasts and the pathogenesis of PF.https://www.mdpi.com/1422-0067/24/10/8749pulmonary fibrosisendothelial cellsendothelial–mesenchymal transitionmyofibroblasts |
| spellingShingle | Weiming Zhao Lan Wang Yaxuan Wang Hongmei Yuan Mengxia Zhao Hui Lian Shuaichen Ma Kai Xu Zhongzheng Li Guoying Yu Injured Endothelial Cell: A Risk Factor for Pulmonary Fibrosis International Journal of Molecular Sciences pulmonary fibrosis endothelial cells endothelial–mesenchymal transition myofibroblasts |
| title | Injured Endothelial Cell: A Risk Factor for Pulmonary Fibrosis |
| title_full | Injured Endothelial Cell: A Risk Factor for Pulmonary Fibrosis |
| title_fullStr | Injured Endothelial Cell: A Risk Factor for Pulmonary Fibrosis |
| title_full_unstemmed | Injured Endothelial Cell: A Risk Factor for Pulmonary Fibrosis |
| title_short | Injured Endothelial Cell: A Risk Factor for Pulmonary Fibrosis |
| title_sort | injured endothelial cell a risk factor for pulmonary fibrosis |
| topic | pulmonary fibrosis endothelial cells endothelial–mesenchymal transition myofibroblasts |
| url | https://www.mdpi.com/1422-0067/24/10/8749 |
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