The role of endothelial-mesenchymal transition in development and pathological process.
Epithelial-mesenchymal transition is an important developmental process, participates in tumor's formation, invasion, and metastasis and has been extensively studied. Recently, endothelial-mesenchymal transition (EndMT), a newly recognized type of cellular transdifferentiation, has been demonstrated to participate in a number of diseases by causing morphology changes and pathological processes. Previous studies showed that EndMT was a critical process of embryonic cardiac development. Not only that recent advances also suggested that EndMT occurred postnatally in cancer and cardiac fibrosis and emerged as a possible source of cancer-associated fibroblasts (CAFs). CAFs were found to acquire properties that promoted tumor development and metastasis formation. Resident endothelial cells undergoing EndMT lose their endothelial markers, acquire a mesenchymal or myofibroblastic phenotype, express mesenchymal cell products such as α-smooth muscle actin and type I collagen and develop invasive and migratory abilities. EndMT-derived cells are believed to function as fibroblasts in damaged tissue and may therefore have an important role in pathological process. However, little is known about the signaling mechanisms that cause endothelial cells to transform into mesenchymal cells. Transforming growth factor-β, Notch, or other signaling pathways could direct or interact to mediate EndMT. Therefore, to explore the signaling mechanisms of EndMT may provide novel therapeutic strategies for treating cancer.
Key Laboratory of Industrial Microbiology, Ministry of Education and Tianjin City, Department of Pharmaceutical Engineering, College of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, China.
Feng
F
Lin
Nan
N
Wang
Tong-Cun
TC
Zhang
D000818:Animals; D054338:Cell Transdifferentiation; D018450:Disease Progression; D047108:Embryonic Development; D005355:Fibrosis; D006331:Heart Diseases / Q000473:pathology*; D006801:Humans; D009369:Neoplasms / Q000473:pathology*; D012038:Regeneration; D015398:Signal Transduction