Endothelial-to-mesenchymal transition pathway (EndoMT pathway)

The **endothelial-to-mesenchymal transition pathway** (EndoMT pathway) is a complex cellular process wherein endothelial cells (which line blood vessels) lose their endothelial identity and acquire mesenchymal characteristics, such as enhanced motility, contractility, and the ability to produce extracellular matrix components[1][4][5]. This transition is driven by signaling pathways including TGF-β, Notch, WNT, and endothelin-1 and involves the activation of key transcription factors (SNAI1, Twist) and broad epigenetic alterations[5][4].\nPhysiologically, EndoMT is essential for embryonic heart development and wound healing but, when dysregulated, contributes to the development and progression of fibrosis, vascular disease, cancer metastasis, and organ failure[2][6].\nThe process can be identified by the loss of endothelial markers (PECAM1/CD31, VE-cadherin) and gain of mesenchymal markers (α-SMA, N-cadherin, FSP-1/S100A4, collagens). While interventions targeting components of the EndoMT-inducing pathways are being explored clinically for fibrosis and cancer, the pathway as a whole is not a single molecular target[5][3].\nSummary:\n- The "endothelial-to-mesenchymal transition pathway" describes a biological *process*, not a distinct drug target. It is *not* a receptor, enzyme, or protein, so use of this entry as a canonical target is incorrect for structured drug annotation purposes. \n- However, modulating the pathway by targeting upstream inducers, transcription factors, or associated molecular events is a focus of ongoing preclinical and clinical research[5][3][6].

Other names

EndMT pathwayEndothelial-to-mesenchymal transitionEndothelial-mesenchymal transitionEndothelial-to-mesenchymal transdifferentiation

Inhibition of TGF-β signaling to block induction of EndoMT\nInterference with Notch, WNT, or endothelin-1 signaling\nEpigenetic modulation to alter EndoMT-associated gene expression\nBlocking transcription factors like SNAI1 or Twist that drive EndoMT