Endothelinkonvertierende

Endothelinkonvertierende, also known as endothelial-to-mesenchymal transition (EndMT), is a biological process where endothelial cells, which line the interior of blood and lymphatic vessels, transition into a mesenchymal-like phenotype. This process is characterized by the loss of endothelial cell-specific markers and the acquisition of mesenchymal markers, such as vimentin and fibronectin. EndMT plays a crucial role in various physiological and pathological conditions, including angiogenesis, wound healing, fibrosis, and cancer metastasis.

The molecular mechanisms underlying EndMT are complex and involve multiple signaling pathways, including transforming growth factor-beta (TGF-beta), Wnt, and Notch signaling. These pathways regulate the expression of transcription factors, such as Snail, Slug, and Twist, which are key mediators of EndMT. The transition from an endothelial to a mesenchymal phenotype is accompanied by changes in cell morphology, loss of cell-cell junctions, and increased migratory and invasive capabilities.

EndMT has been extensively studied in the context of cancer, where it contributes to tumor progression and metastasis. Endothelial cells in tumor vessels undergo EndMT, leading to the formation of a mesenchymal-like phenotype that promotes tumor growth and invasion. Additionally, EndMT has been implicated in the development of fibrosis, a condition characterized by excessive deposition of extracellular matrix in various organs. In fibrosis, EndMT contributes to the activation of fibroblasts and the production of collagen, leading to tissue scarring and organ dysfunction.

In summary, endothelinkonvertierende is a dynamic process that involves the transition of endothelial cells into a mesenchymal-like phenotype. This process is regulated by multiple signaling pathways and plays a critical role in various physiological and pathological conditions, including angiogenesis, wound healing, fibrosis, and cancer metastasis. Further research is needed to fully understand the molecular mechanisms underlying EndMT and to develop targeted therapeutic strategies to modulate this process in disease.