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FSTL1通过增强细胞自噬促进COPD的气道炎症与气道重塑.docx

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FSTL1通过增强细胞自噬促进COPD的气道炎症与气道重塑 FSTL1(Follistatin-like1)isasecretedglycoproteinthatplaysasignificantroleinvariousbiologicalprocesses,includingcellproliferation,differentiation,andinflammation.RecentresearchhassuggestedthatFSTL1mayalsocontributetothepathogenesisofchronicobstructivepulmonarydisease(COPD),adebilitatinglungconditioncharacterizedbypersistentairflowlimitation,inflammation,andremodelingoftheairways. COPDisaleadingcauseofmorbidityandmortalityworldwide,affectingmillionsofindividuals.TheprimaryriskfactorforCOPDiscigarettesmoking,althoughotherenvironmentalandgeneticfactorsalsocontributetoitsdevelopment.TheelucidationoftheunderlyingmechanismsinvolvedinCOPDpathogenesisiscrucialforthedevelopmentofnoveltherapeuticstrategies. Autophagy,ahighlyconservedcellularprocess,isresponsibleforthedegradationofdysfunctionalcellularcomponentsandtherecyclingofcellularmaterials.Studieshaveshowndysregulationofautophagyinvariouslungdiseases,includingCOPD.FSTL1hasbeenidentifiedasapotentregulatorofautophagy,suggestingapotentialroleinCOPDpathogenesis. SeverallinesofevidencesupporttheinvolvementofFSTL1inpromotingairwayinflammationinCOPD.Firstly,FSTL1expressionissignificantlyincreasedinbronchialepithelialcellsandlungtissueofCOPDpatients.ThisupregulationofFSTL1appearstobemediatedbypro-inflammatorycytokines,suchastumornecrosisfactor-alpha(TNF-α)andinterleukin-1beta(IL-1β).Secondly,animalstudieshavedemonstratedthatoverexpressionofFSTL1leadstoenhancedairwayinflammation,characterizedbyincreasedinfiltrationofinflammatorycellsandpro-inflammatorycytokineproduction.Conversely,FSTL1knockoutorknockdownreducesairwayinflammationinexperimentalmodelsofCOPD. Inadditiontopromotinginflammation,FSTL1hasalsobeenimplicatedinairwayremodeling,akeyfeatureofCOPD.Airwayremodelingreferstothestructuralchangesintheairwaywall,includingincreasedsmoothmusclemass,epithelialalterations,anddepositionofextracellularmatrixcomponents.StudieshaveshownthatFSTL1caninducetheexpressionofmatrixmetalloproteinases(MMPs)andtheproducti