Stanford-A acute aortic dissection, inflammation, and metalloproteinases: A review

Cifani, Noemi; Proietta, Maria; Tritapepe, Luigi; Gioia, Cira Di; Ferri, Livia; Taurino, Maurizio; Porto, Flavia Del

doi:10.3109/07853890.2015.1073346

Cited by 113 publications

(119 citation statements)

References 70 publications

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“…Furthermore, increased neutrophils, macrophages, and MMP-9 have been detected in aortic tissue or blood of patients with AD (14-17). MMP-9, which degrades elastin and collagens, can be produced by neutrophils, macrophages, or vascular smooth muscle cells (16,18). Our studies using adoptive transfer of WT or LNK-deficient leukocytes into Rag1 -/mice demonstrate that loss of LNK in immune cells plays a key role in development of AD ( Figure 4) and that Lnk -/neutrophils secrete more MMP-9 when activated ex vivo and exhibit increased migratory capacity in the setting of Ang II infusion ( Figure 5, D and E).…”

Section: Discussionmentioning

confidence: 99%

LNK deficiency promotes acute aortic dissection and rupture

Laroumanie¹,

Korneva²,

Bersi³

et al. 2018

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Section: Discussionmentioning

confidence: 99%

LNK deficiency promotes acute aortic dissection and rupture

Laroumanie¹,

Korneva²,

Bersi³

et al. 2018

JCI Insight

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“…1) It is classified as Stanford type A when the ascending aortic thoracic tract is involved and Stanford type B when the descending thoracic aorta is targeted. 2,3) As the most common thoracic aortic emergency, AAD may be rapidly fatal without early diagnosis and appropriate management, 4) and it may be associated with giant cell arteritis.…”

mentioning

confidence: 99%

Biomarkers Investigation for In-Hospital Death in Patients With Stanford Type A Acute Aortic Dissection

et al. 2016

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SummaryThis retrospective study aimed to investigate the predictive value of biomarkers for in-hospital mortality of patients with Stanford type A acute aortic dissection (AAD).AAD is a life-threatening disease with an incidence of about 2.6-3.6 cases per 100,000/year. A total of 67 consecutive Stanford type A AAD patients admitted to hospital were divided into a deceased group and survival group. The baseline information of the patients between two groups was systematically compared, followed by examination of the electrocardiograms (ECG). Based on the follow-up during hospitalization, we investigated the simultaneous assessment of indexes like fragmented QRS complex (fQRS), admission systolic blood pressure (SBP), aortic diameter, surgical management, troponin I (TnI), white blood cell (WBC) count, N-terminal pro-brain natriuretic peptide (NT-proBNP), and D-dimer.The levels of TnI and NT-proBNP, WBC counts, and rate of fQRS (+) in patients of the deceased group were significantly higher than those in the survival group. The male sex (hazard ratio, 10.88; P = 0.001), admission SBP (hazard ratio, 0.98; P = 0.012), NT-proBNP (hazard ratio, 1.00; P = 0.001), and WBC count (hazard ratio, 1.10; P = 0.033) were independently related with in-hospital death. As a single marker, WBC count had the highest sensitivity at 84.6% (specificity 65.9%).Admission SBP, NT-proBNP, and WBC count were potential independent risk factors of in-hospital death in Stanford type A AAD patients. WBC count may be a more accurate predictor of type A AAD than either alone. (Int Heart J 2016; 57: 622-626)

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“…Studies in human AD samples and animal AD models indicate that inflammatory response plays a central role in the pathogenesis of AD [3,4]. We also reported the involvement of inflammatory response in mouse models [5][6][7] and in human AD tissue [8].…”

Section: Introductionmentioning

confidence: 58%

“…As the transcriptome analysis suggested that MRTF-A regulates the inflammatory response that plays a central role in AD pathogenesis [3,4], we performed quantitative analysis of inflammatory cytokines by qRT-PCR in aortic tissue (Fig 4). The mRNA expressions of Il6 and Ccl2 were induced by 1 day of AngII infusion in WT aorta, while this response was not observed in MRTF-A-KO mice (Fig 4A).…”

Section: Role Of Mrtf-a In Aortic Wall Inflammation and Apoptosismentioning

confidence: 99%

MRTF-A promotes angiotensin II-induced inflammatory response and aortic dissection in mice

et al. 2020

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Aortic dissection (AD) is a major cause of acute aortic syndrome with high mortality due to the destruction of aortic walls. Although recent studies indicate the critical role of inflammation in the disease mechanism of AD, it is unclear how inflammatory response is initiated. Here, we demonstrate that myocardin-related transcription factor A (MRTF-A), a signal transducer of humoral and mechanical stress, plays an important role in pathogenesis of AD in a mouse model. A mouse model of AD was created by continuous infusion of angiotensin II (AngII) that induced MRTF-A expression and caused AD in 4 days. Systemic deletion of Mrtfa gene resulted in a marked suppression of AD development. Transcriptome and gene annotation enrichment analyses revealed that AngII infusion for 1 day caused pro-inflammatory and pro-apoptotic responses before AD development, which were suppressed by Mrtfa deletion. AngII infusion for 1 day induced pro-inflammatory response, as demonstrated by expressions of Il6, Tnf, and Ccl2, and apoptosis of aortic wall cells, as detected by TUNEL staining, in an MRTF-A-dependent manner. Pharmacological inhibition of MRTF-A by CCG-203971 during AngII infusion partially suppressed AD phenotype, indicating that acute suppression of MRTF-A is effective in preventing the aortic wall destruction. These results indicate that MRTF-A transduces the stress of AngII challenge to the pro-inflammatory and proapoptotic responses, ultimately leading to AD development. Intervening this pathway may represent a potential therapeutic strategy.

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Stanford-A acute aortic dissection, inflammation, and metalloproteinases: A review

Cited by 113 publications

References 70 publications

LNK deficiency promotes acute aortic dissection and rupture

LNK deficiency promotes acute aortic dissection and rupture

Biomarkers Investigation for In-Hospital Death in Patients With Stanford Type A Acute Aortic Dissection

MRTF-A promotes angiotensin II-induced inflammatory response and aortic dissection in mice

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