Adenosinetriphosphate(ATP)isthemostabundantandprimarycarrieroftherequiredenergyforvariousfunctionsincells.Prolongedischemia,reperfusion,anaerobicmetabolismandlactateaccumulationcanleadtoadramaticdecreaseofATP,cellswelling,cellrupture,andfinallycelldeathbynecrotic,necroptotic,apoptotic,andautophagicmechanisms. DuetodrastichydrolysisofATP invivo byectoenzymesandpoorcellularpenetration,thedirectdeliveryofATPtotheischemictissuesisdifficult.

ToincreasedeliveryofATPtothetissuesandprotectfromenzymaticdegradation,encapsulationinliposomeshasbeenproposedanddemonstratedinvariousmodelsofischemia[1,2]. Studiesonmyocardial[1,3,4], liver[5-8], retina[9] andwoundhealing[10-12] ischemiahaveshowntheABIlityofLiposomalencapsulatedATPtopreventcelldeathandtissuedysfunctionfollowingischemicevents.

TheencapsulationofATPinliposomesmarkedlypromotesitseffectivenessbypreventingthehydrolysisbyextracellularenzymes,increasingATPcirculationtimeandenhancingitsintracellularpenetration.Dependingonthetypeofthecelllineandthetargetorganvarioustypesofliposomeswithdifferentsurfacechargessuchasanionic,cationicandneutralhasbeenstudiedbyvariousgroups.Moreover,ATPencapsulatedliposomeshasbeendemonstratedtoimproveenergystateandfunctionofthecold-storedliver[6,7,13].