Glutaminolysisisacriticalmetabolicpathwaythatsupportsendothelialcellfunctionbyprovidingenergyandbiosyntheticprecursors.Recentstudieshavedemonstratedthattransforminggrowthfactor-beta1(TGF-β1)caninduceglutaminolysisinendothelialcellsthroughaspecificsignalingcascade.Thisprocessinvolvestheproteinphosphatase2Acatalyticsubunit(PP2Ac),whichregulatestheRAF-MEK-ERKsignalingpathway.TheactivationofthispathwaybyTGF-β1promotesglutaminemetabolism,therebyinfluencingendothelialcellbehavior,includingproliferation,migration,andangiogenesis.Understandingthismechanismprovidesinsightsintothemetabolicreprogrammingofendothelialcellsunderphysiologicalandpathologicalconditions,suchaswoundhealing,inflammation,andtumorangiogenesis.Furtherresearchinthisareamayrevealpotentialtherapeutictargetsfordiseasesinvolvingaberrantendothelialcellmetabolism.
