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1、REVIEWSAutophagymodulationasapotentialtherapeutictargetfordiversediseasesDavidC. Rubinsztein1*,PatriceCodogno2*andBethLevine3*Abstract
2、Autophagyisanessential,conservedlysosomaldegradationpathwaythatcontrolsthequalityofthecytoplasmbyeliminatingproteinaggregatesanddamagedorganelles
3、.Itbeginswhendouble-membranedautophagosomesengulfportionsofthecytoplasm,whichisfollowedbyfusionofthesevesicleswithlysosomesanddegradationoftheautophagiccontents.Inadditiontoitsvitalhomeostaticrole,thisdegradationpathwayisinvolvedinvarioushumandisorders,includingmetaboliccondition
4、s,neurodegenerativediseases,cancersandinfectiousdiseases.Thisarticleprovidesanoverviewofthemechanismsandregulationofautophagy,theroleofthispathwayindiseaseandstrategiesfortherapeuticmodulation.Autophagyoccursatabasalrateinmostcells,eliminatingcasesautophagicactivitymaybepermissiv
5、etowardsAutophagosomesDouble-membranevesiclesproteinaggregatesanddamagedorganellesinordertopathogenesis.Inaddition,theinductionofautophagymaintaincytoplasmichomeostasis1.Thisincludesthedeg-hasbeenshowntoincreaselongevityinalargepanelofthatengulfcytoplasmiccontentsfordeliverytothe
6、radationofdysfunctionalmitochondriaviamitophagy,species(reviewedinREF. 9),thusraisingthepossibilitylysosome.acytoprotectiveprocessthatlimitsboththeproductionthatageingandlongevitymaybetherapeutictargetsforofreactiveoxygenspecies(ROS)andthereleaseoftoxicautophagyinduction.intramit
7、ochondrialproteins.Giventheseobservations,pharmacologicalapproaches1DepartmentofMedicalAutophagyisstimulatedduringvariouspathologicaltoupregulateorinhibitthispathwayarecurrentlyreceivingGenetics,CambridgeInstituteandphysiologicalstates,suchasstarvation.Starvation-considerableatte
8、ntion.Forexample,autophagyupregula-forMedicalResearch,inducedautophagy,anevolutionarilyconservedresponsetionmaybeoftherapeuticbenefitincertainneurodegen-UniversityofCambridge,ineukaryotes2,enablesthedegradationofproteins,erativediseases(suchasHuntington’sdisease),whereasWellcomeT
9、rust/MRCcarbohydratesandlipids,whichallo
