血管平滑肌細(xì)胞在胸主動(dòng)脈瘤及夾層發(fā)生發(fā)展中的作用

中圖分類(lèi)號(hào)：R543 文獻(xiàn)標(biāo)志碼：A 文章編號(hào)：1001-5779（2025）05-0429-05

DOI：10.3969/j.issn. 1001-5779.2025.05.003

Abstract：Thoracicaorticaneurysmand dissectionsrepresent agroupof clinicallprevalentcardiovasculardisorders characterizedbyprogressivedilationof theaorticwall.Itspathogenesisremainsincompletelyunderstood.Anatomicaly， the aorticwallconsistsof threelayers，with vascularsmooth musclecelsbeing the principal constituentof the midle layer.Thisreviewsynthesizesrecent domesticand internationalliterature toexaminethemechanisticcontributionsof vascularsmooth muscle cels toaortic wallpathologyand dissection development，while evaluating targeted preventive andtherapeutic strategies directedat thesecells.The findingsdemonstrate thatthoracicaorticaneurysmand dissection pathogenesis induces phenotypic switching of vascular smooth musclecells into functionally diversesubtypes.These transformedcells exhibit dual functionality：theyrespond to neural stimuli bysecreting growth factorsand cytokines including MMP，TGF- β and TNF- α that modulate disease progression，while simultaneously releasing collagen to facilitate aorticremodeling and repair.Therapeutic interventions for thoracic aortic aneurysmsand dissections must prioritize inhibitionofkey genetic regulators governing vascularsmooth musclecellphenotypic transition，particularlyupstreamand downstream mediatorssuchas MEKK2/3，ALDH2 and ANXA1.

KeyWords：Thoracicaorticaneurysms；Thoracicaortic dissections；Vascular smooth musclecells；Pathogenesis； Targeted therapy

胸主動(dòng)脈瘤是一種極其危險(xiǎn)的心血管疾病，由于各種因素導(dǎo)致的主動(dòng)脈壁中層強(qiáng)度進(jìn)行性減弱，進(jìn)而逐漸擴(kuò)張，當(dāng)擴(kuò)張到一定程度后主動(dòng)脈內(nèi)膜被血流撕裂形成破口，血流進(jìn)入破口，剝離主動(dòng)脈壁內(nèi)血管結(jié)構(gòu)，在主動(dòng)脈內(nèi)膜與中外膜之間形成假腔，稱(chēng)為主動(dòng)脈夾層。（剩余10887字）