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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Main Authors: Cheng Qian, Guanglu Dong, Chunmei Yang, Weiwei Zheng, Chongjin Zhong, Qiuhong Shen, Yin Lu, Yang Zhao
Format: Article
Language:English
Published: BMC 2025-01-01
Series:Cell Communication and Signaling
Subjects:
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.
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institution Kabale University
issn 1478-811X
language English
publishDate 2025-01-01
publisher BMC
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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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