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MALAT1在LPS诱导的炎症反应中的功能与机制研究.docx

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MALAT1在LPS诱导的炎症反应中的功能与机制研究 Title:TheFunctionalMechanismsofMALAT1inLPS-InducedInflammatoryResponse Abstract: Longnon-codingRNAs(lncRNAs)haveemergedascriticalregulatorsinvariouscellularprocesses,includinginflammation.OnesuchlncRNAisMALAT1(Metastasis-AssociatedLungAdenocarcinomaTranscript1),whichhasbeenimplicatedinmultiplephysiologicalandpathologicalprocesses.Inthisreview,weaimtosummarizethecurrentunderstandingofthefunctionalmechanismsofMALAT1inlipopolysaccharide(LPS)-inducedinflammatoryresponse.WewilldiscusstherolesofMALAT1inregulatinginflammatorygeneexpression,modulatingimmunecellfunctions,andregulatingsignalingpathwaysinvolvedintheLPS-inducedinflammatoryresponse.Furthermore,wewillhighlightthepotentialtherapeuticapplicationsoftargetingMALAT1inthetreatmentofinflammatorydiseases. Introduction: Inflammationisacrucialdefensemechanismoftheimmunesystemagainstpathogensandtissuedamage.However,dysregulatedorchronicinflammationcancontributetothepathogenesisofvariousinflammatorydiseases,includingsepsis,inflammatoryboweldisease,andrheumatoidarthritis.Understandingtheregulatorymechanismsofinflammationiscrucialforthedevelopmentofeffectivetherapeuticstrategies.Recently,lncRNAshavebeenrecognizedasimportantregulatorsofgeneexpressionandcellularfunctions.AmongtheselncRNAs,MALAT1hasgarneredsignificantattentionduetoitsdiverserolesinvariousbiologicalprocesses,includinginflammation. MALAT1andInflammatoryGeneExpression: MALAT1hasbeenshowntoregulatetheexpressionofvariousinflammatorygenesinresponsetoLPSstimulation.SeveralstudieshavedemonstratedthatMALAT1expressionissignificantlyincreasedinLPS-treatedcellsortissues.Mechanistically,MALAT1caninteractwithtranscriptionfactorsorepigeneticmodifierstomodulatetheexpressionoftargetgenesinvolvedintheinflammatoryresponse.Forexample,MALAT1candirectlybindtoandsequesterthetranscriptionfactorNF-κB,preventingitsnucleartranslocationandsubsequentactivationofpro-inflammatorygeneexpression.Additionally,MALAT1canrecruitandinteractwiththehistonemethyltransferaseEnh