Abstract
Endothelial to mesenchymal transition (EndMT) is a complex biological process that gives rise to cells with multipotent potential. EndMT is essential for the formation of the cardiovascular system during embryonic development. Emerging results link EndMT to the postnatal onset and progression of fibrotic diseases and cancer. Moreover, recent reports have emphasized the potential for EndMT in tissue engineering and regenerative applications by regulating the differentiation status of cells. Transforming growth factor β (TGF-β) engages in many important physiological processes and is a potent inducer of EndMT. In this review, we first summarize the mechanisms of the TGF-β signaling pathway as it relates to EndMT. Thereafter, we discuss the pivotal role of TGF-β-induced EndMT in the development of cardiovascular diseases, fibrosis, and cancer, as well as the potential application of TGF-β-induced EndMT in tissue engineering.
Highlights
The cardiovascular system has the supportive role of supplying oxygen and nutrition to the whole body and simultaneously removes toxic waste products from tissues and organs through an extensive and intricated network of blood vessels
Whether endothelial cells (ECs) contribute to ectopic bone formation in Fibrodysplasia ossificans progressiva (FOP) patients remains controversial, we have recently demonstrated how circulating ECs isolated from FOP donors exhibit enhanced endothelial to mesenchymal transition (EndMT) and osteogenic differentiation in vitro, which was used as a functional readout to identify novel small molecules targeting ALK2 (Sánchez-Duffhues et al, 2019b)
Transforming growth factor β (TGF-β) stimulation could induce EndMT as vimentin/smooth muscle protein 22α (SM22α) was expressed in Isolectin B4 stained ECs, and more vascularization was observed in cardiac tissue mimetics (CTMs)
Summary
The cardiovascular system has the supportive role of supplying oxygen and nutrition to the whole body and simultaneously removes toxic waste products from tissues and organs through an extensive and intricated network of blood vessels. TGF-β family members trigger biological processes by inducing the formation of cell surface receptor complexes bearing intrinsic serine/threonine kinase activity. TGF-β family members mediate EndMT via Smad or nonSmad signaling propagated by inducing the expression of specific transcription factors, such as Snail, Slug, Twist, ZEB1, SIP1/ZEB2, and LEF-1 (Yoshimatsu and Watabe, 2011).
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