TUhjnbcbe - 2021/7/4 21:48:00
TODAY今日发布CardiovascDiabetolDec01,:18(1)今日发布01篇（共计篇）JAHANov05,:8(21)今日发布11篇（共计20篇）JAMAEarlyRecent,Oct18,今日发布02篇HerzEarlyRecent,Oct18,今日发布01篇NethHeartJEarlyRecent,Oct18,今日发布01篇HeartandVesselsEarlyRecent,Oct18,今日发布01篇RECOMMEND推荐阅读01CTRP9改善心肌梗死后大鼠的心房炎症、纤维化和房颤易感性JAHAresearch-articleMingxinLiu,WeiLi,etc.2小时前等16用户推荐阅读本文BackgroundInflammationandfibrosisplayanimportantroleinthepathogenesisofatrialfibrillation(AF)aftermyocardialinfarction(MI).CTRP9(C1q/tumornecrosisfactor‐relatedprotein‐9)asasecretedglycoproteincanreverseleftventricleremodelingpost‐MI,butitseffectsonMI‐inducedatrialinflammation,fibrosis,andassociatedAFareunknown.炎症和纤维化在心肌梗死（mi）后心房颤动（af）的发病机制中起重要作用。ctrp9（c1q/tumornecrosisfactor-relatedprotein-9）作为一种分泌性糖蛋白可以逆转心肌梗死后左室重构，但其对心肌梗死引起的心房炎症、纤维化和相关房颤的影响尚不清楚。MethodsandResultsMImodelratsreceivedadenoviralsupplementationofCTRP9(Ad‐CTRP9)byjugular‐veininjection.Cardiacfunction,inflammatory,andfibroticindexesandrelatedsignalingpathways,electrophysiologicalproperties,andAFinducibilityofatriainvivoandexvivoweredetectedin3or7daysafterMI.shCTRP9(shorthairpinCTRP9)andshRNAwereinjectedintoratandperformedsimilardetectionatday5or10.Adverseatrialinflammationandfibrosis,cardiacdysfunctionwereinducedinbothMIandAd‐GFP(adenovirus‐encodinggreenfluorescentprotein)MIrats.SystemicCTRP9treatmentimprovedcardiacdysfunctionpost‐MI.CTRP9markedlyamelioratedmacrophageinfiltrationandattenuatedtheinflammatoryresponsesbydownregulatinginterleukin‐1βandinterleukin‐6,andupregulatinginterleukin‐10,in3dayspost‐MI;depressedleftatrialfibrosisbydecreasingtheexpressionsofcollagentypesIandIII,α‐SMA,andtransforminggrowthfactorβ1in7dayspost‐MIpossiblythroughdepressingtheToll‐likereceptor4/nuclearfactor‐κBandSmad2/3signalingpathways.ElectrophysiologicrecordingsshowedthatincreasedAFinducibilityandduration,andprolongationofinteratrialconductiontimeinducedbyMIwereattenuatedbyCTRP9;moreover,CTRP9wasnegativelycorrelatedwithinterleukin‐1βandAFduration.DownregulationofCTRP9aggravatedatrialinflammation,fibrosis,susceptibilityofAFandprolongedinteratrialconductiontime,withoutaffectingcardiacfunction.mi模型大鼠经颈静脉注射腺病*补充剂ctrp9（ad-ctrp9）。分别于心肌梗死后3、7天检测心功能、炎症、纤维化指标及相关信号传导途径、电生理特性和心房纤颤诱导率。将SHCTRP9（短发夹CTRP9）和SHRNA注入大鼠体内，在第5天或第10天进行类似检测。在心肌梗死和ad-gfp（腺病*编码绿色荧光蛋白）心肌梗死大鼠中均诱发了不良的心房炎症和纤维化、心功能不全。全身CTRP9治疗改善心肌梗死后心功能不全。心肌梗死后3天，CTRP9通过下调白细胞介素-1β和白细胞介素-6，上调白细胞介素-10，显著改善巨噬细胞浸润，减轻炎症反应；通过降低I型和III型胶原、α-SMA的表达，抑制左房纤维化。心肌梗死后7天转化生长因子β1可能通过抑制toll样受体4/nuclearfactor-κb和smad2/3信号传导途径实现。电生理记录显示，ctrp9能减弱心肌梗死诱导的房颤发生率和持续时间的增加，并能延长房颤的室间传导时间，而且ctrp9与白细胞介素1β和房颤持续时间呈负相关。CTRP9下调可加重心房炎症、纤维化、房颤易感性和延长心房传导时间，但不影响心功能。ConclusionsCTRP9iseffectiveatattenuatingatrialinflammationandfibrosis,possiblyviaitsinhibitoryeffectsontheToll‐likereceptor4/nuclearfactor‐κBandSmad2/3signalingpathways,andmaybeanoriginalupstreamtherapyforAFinearlyphaseofMI.CTRP9可能通过抑制Toll样受体4/核因子-κB和Smad2/3信号通路而有效地减轻心房炎症和纤维化，可能是心肌梗死早期心房颤动的一种原始上游疗法。Atrialfibrillation(AF)isanincreasingly