Endothelial-to-mesenchymal transition process (EndoMT)

Endothelial-to-mesenchymal transition (EndoMT) is a biologically significant process whereby endothelial cells gradually lose their unique markers and characteristics, and acquire mesenchymal traits, such as enhanced motility, contractility, and the ability to produce extracellular matrix proteins. This process plays a vital role in heart development and tissue repair but, when dysregulated, contributes to diseases including fibrosis, cancer, and cardiovascular pathologies. The transition is driven by multiple signaling pathways, most notably transforming growth factor-β (TGF-β). Therapeutically, modulating EndoMT is complex: inhibiting the process may limit pathological fibrosis or tumor progression, but may also impair necessary physiological responses. Note: The target as named ("Endothelial-to-mesenchymal transition process") is not a molecule/receptor, so is not considered a conventional therapeutic target. Instead, its cellular regulators or signaling pathways are typically the focus of therapeutic intervention.

Other names

EndoMTendothelial-mesenchymal transition

Inhibition/modulation of signaling pathways (e.g., TGF-β, Notch, Wnt, BMP) that drive EndoMT. Anti-inflammatory agents or fibrosis-targeting drugs may decrease EndoMT indirectly via their action on upstream signals.