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Front. Immunol. | doi: 10.3389/fimmu.2018.00294

Endothelial to Mesenchymal Transition is a Fundamental Component in the Interaction between Inflammatory Processes and Endothelial Dysfunction

 Jin Gu Cho1, Aram Lee1,  Woochul Chang2, Myeong-Sok Lee1 and  Jongmin Kim1*
  • 1Sookmyung Women's University, South Korea
  • 2Department of Biology Education, College of Education, Pusan National University, South Korea

Endothelial cells that line the inner walls of blood vessels are in direct contact with blood and display remarkable heterogeneity in their response to exogenous stimuli. These endothelial cells have unique location-dependent properties determined by the corresponding vascular beds and play an important role in regulating the homeostasis of the vascular system. Evidence suggests that vascular endothelial cells exposed to various environments undergo dynamic phenotypic switching, a key biological program in the context of endothelial heterogeneity, but that might result in endothelial cell dysfunction and, in turn, cause a variety of human diseases. Emerging studies show the importance of endothelial to mesenchymal transition (EndMT) in endothelial dysfunction during inflammation. EndMT is a complex biological process in which endothelial cells lose their endothelial characteristics, acquire mesenchymal phenotypes, and express mesenchymal cell markers such as alpha smooth muscle actin and fibroblast specific protein 1. EndMT is induced by inflammatory responses, leading to pathological states, including tissue fibrosis, pulmonary arterial hypertension, and atherosclerosis, via dysfunction of the vascular system. Although the mechanisms associated with inflammation-induced EndMT have been identified, unraveling the specific role of this phenotypic switching in vascular dysfunction remains a challenge. Here, we review the current understanding on the interactions between inflammatory processes, EndMT, and endothelial dysfunction, with a focus on the mechanisms that regulate essential signaling pathways. Identification of such mechanisms will guide future research and could provide novel therapeutic targets for the treatment of vascular diseases.

Keywords: endothelial dysfunction, Inflammatory process, Endothelial to mesenchymal transition, endothelial heterogeneity, vascular disease

Received: 23 Oct 2017; Accepted: 01 Feb 2018.

Edited by:

Olaf Penack, Charité Universitätsmedizin Berlin, Germany

Reviewed by:

Claudia Penna, Università degli Studi di Torino, Italy
Adriana Georgescu, Institute of Cellular Biology and Pathology (ICBP), Romania  

Copyright: © 2018 Cho, Lee, Chang, Lee and Kim. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Prof. Jongmin Kim, Sookmyung Women's University, Seoul, 04310, South Korea, jkim@sookmyung.ac.kr