Injured Endothelial Cell: A Risk Factor for Pulmonary Fibrosis

Author:

Zhao Weiming1,Wang Lan1,Wang Yaxuan1,Yuan Hongmei1,Zhao Mengxia1,Lian Hui1,Ma Shuaichen1,Xu Kai1,Li Zhongzheng1,Yu Guoying1ORCID

Affiliation:

1. State 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, China

Abstract

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.

Funder

Ministry of Science and Technology

State Innovation Base for Pulmonary Fibrosis

Henan Project of Science and Technology

Xinxiang Major Project

Publisher

MDPI AG

Subject

Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis

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