Broadening horizons: molecular mechanisms and disease implications of endothelial-to-mesenchymal transition
Abstract Endothelial-mesenchymal transition (EndMT) is defined as an important process of cellular differentiation by which endothelial cells (ECs) are prone to lose their characteristics and transform into mesenchymal cells. During EndMT, reduced expression of endothelial adhesion molecules disrupt...
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Language: | English |
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BMC
2025-01-01
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Series: | Cell Communication and Signaling |
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Online Access: | https://doi.org/10.1186/s12964-025-02028-y |
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author | Cheng Qian Guanglu Dong Chunmei Yang Weiwei Zheng Chongjin Zhong Qiuhong Shen Yin Lu Yang Zhao |
author_facet | Cheng Qian Guanglu Dong Chunmei Yang Weiwei Zheng Chongjin Zhong Qiuhong Shen Yin Lu Yang Zhao |
author_sort | Cheng Qian |
collection | DOAJ |
description | Abstract Endothelial-mesenchymal transition (EndMT) is defined as an important process of cellular differentiation by which endothelial cells (ECs) are prone to lose their characteristics and transform into mesenchymal cells. During EndMT, reduced expression of endothelial adhesion molecules disrupts intercellular adhesion, triggering cytoskeletal reorganization and mesenchymal transition. Numerous studies have proved that EndMT is a multifaceted biological event driven primarily by cytokines such as TGF-β, TNF-α, and IL-1β, alongside signaling pathways like WNT, Smad, MEK-ERK, and Notch. Nevertheless, the exact roles of EndMT in complicated diseases have not been comprehensively reviewed. In this review, we summarize the predominant molecular regulatory mechanisms and signaling pathways that contribute to the development of EndMT, as well as highlight the contributions of a series of imperative non-coding RNAs in curbing the initiation of EndMT. Furthermore, we discuss the significant impact of EndMT on worsening vasculature-related diseases, including cancer, cardiovascular diseases, atherosclerosis, pulmonary vascular diseases, diabetes-associated fibrotic conditions, and cerebral cavernous malformation, providing the implications that targeting EndMT holds promise as a therapeutic strategy to mitigate disease progression. |
format | Article |
id | doaj-art-e1fc7edc190149fc9c2be1cfb1c3a4a8 |
institution | Kabale University |
issn | 1478-811X |
language | English |
publishDate | 2025-01-01 |
publisher | BMC |
record_format | Article |
series | Cell Communication and Signaling |
spelling | doaj-art-e1fc7edc190149fc9c2be1cfb1c3a4a82025-01-12T12:32:59ZengBMCCell Communication and Signaling1478-811X2025-01-0123112110.1186/s12964-025-02028-yBroadening horizons: molecular mechanisms and disease implications of endothelial-to-mesenchymal transitionCheng Qian0Guanglu Dong1Chunmei Yang2Weiwei Zheng3Chongjin Zhong4Qiuhong Shen5Yin Lu6Yang Zhao7School of Medicine, Nanjing University of Chinese MedicineSchool of Medicine, Nanjing University of Chinese MedicineSchool of Medicine, Nanjing University of Chinese MedicineSchool of Medicine, Nanjing University of Chinese MedicineSchool of Medicine, Nanjing University of Chinese MedicineSchool of Medicine, Nanjing University of Chinese MedicineJiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Materia Medica, Jiangsu Joint International Research Laboratory of Chinese Medicine and Regenerative Medicine, Nanjing University of Chinese MedicineSchool of Medicine, Nanjing University of Chinese MedicineAbstract Endothelial-mesenchymal transition (EndMT) is defined as an important process of cellular differentiation by which endothelial cells (ECs) are prone to lose their characteristics and transform into mesenchymal cells. During EndMT, reduced expression of endothelial adhesion molecules disrupts intercellular adhesion, triggering cytoskeletal reorganization and mesenchymal transition. Numerous studies have proved that EndMT is a multifaceted biological event driven primarily by cytokines such as TGF-β, TNF-α, and IL-1β, alongside signaling pathways like WNT, Smad, MEK-ERK, and Notch. Nevertheless, the exact roles of EndMT in complicated diseases have not been comprehensively reviewed. In this review, we summarize the predominant molecular regulatory mechanisms and signaling pathways that contribute to the development of EndMT, as well as highlight the contributions of a series of imperative non-coding RNAs in curbing the initiation of EndMT. Furthermore, we discuss the significant impact of EndMT on worsening vasculature-related diseases, including cancer, cardiovascular diseases, atherosclerosis, pulmonary vascular diseases, diabetes-associated fibrotic conditions, and cerebral cavernous malformation, providing the implications that targeting EndMT holds promise as a therapeutic strategy to mitigate disease progression.https://doi.org/10.1186/s12964-025-02028-yEndothelial-mesenchymal transitionEndothelial cellsMesenchymal phenotypeNon-coding RNATGF-β signaling pathway |
spellingShingle | Cheng Qian Guanglu Dong Chunmei Yang Weiwei Zheng Chongjin Zhong Qiuhong Shen Yin Lu Yang Zhao Broadening horizons: molecular mechanisms and disease implications of endothelial-to-mesenchymal transition Cell Communication and Signaling Endothelial-mesenchymal transition Endothelial cells Mesenchymal phenotype Non-coding RNA TGF-β signaling pathway |
title | Broadening horizons: molecular mechanisms and disease implications of endothelial-to-mesenchymal transition |
title_full | Broadening horizons: molecular mechanisms and disease implications of endothelial-to-mesenchymal transition |
title_fullStr | Broadening horizons: molecular mechanisms and disease implications of endothelial-to-mesenchymal transition |
title_full_unstemmed | Broadening horizons: molecular mechanisms and disease implications of endothelial-to-mesenchymal transition |
title_short | Broadening horizons: molecular mechanisms and disease implications of endothelial-to-mesenchymal transition |
title_sort | broadening horizons molecular mechanisms and disease implications of endothelial to mesenchymal transition |
topic | Endothelial-mesenchymal transition Endothelial cells Mesenchymal phenotype Non-coding RNA TGF-β signaling pathway |
url | https://doi.org/10.1186/s12964-025-02028-y |
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