Serum amyloid a protein as a potential biomarker in predicting acute onset and association with in-hospital death in acute aortic dissection

He, Yuchen; Ma, Chang-cheng; Xing, Jia; Wang, Shiyue; Ji, Chao; Han, Yanshuo; Zhang, Jian

doi:10.1186/s12872-019-1267-0

Cited by 14 publications

(8 citation statements)

References 34 publications

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“…41 In agreement with previous observations that recombinant CCN2 stimulated migration and proliferation of rat VSMCs, 42 Ccn2 deletion decreased wound healing and cell migration in cultured murine VSMCs. Our RNA-seq study showed that Ang II increased the aortic expression of Saa3, S100a8, S100a9, and Ccl8, which are all involved in vascular damage and inflammation, [43][44][45][46] and that CCN2 deficiency resulted in even higher expression of these genes, supporting a potential role in aneurysm formation. Elevated SAA and S100A8/S100A9 complexes were observed in human cardiovascular diseases including acute aortic dissection, aneurysms, or atherosclerosis.…”

Section: Discussionmentioning

confidence: 62%

“…Elevated SAA and S100A8/S100A9 complexes were observed in human cardiovascular diseases including acute aortic dissection, aneurysms, or atherosclerosis. 46,47 Moreover, Saa deficiency protected ApoE −/− mice from Ang II-induced abdominal aortic aneurysm formation. 48 Interestingly, the systemic administration of a high dose of CCN2-IV failed in preventing aneurysm formation and rupture, suggesting that endogenous, local CCN2 expression is essential for the proper function, maintenance, and adaptive responses of the aortic vascular wall.…”

Section: Discussionmentioning

confidence: 96%

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CCN2 (Cellular Communication Network Factor 2) Deletion Alters Vascular Integrity and Function Predisposing to Aneurysm Formation

et al. 2022

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Background: CCN2 (cellular communication network factor 2) is a matricellular protein involved in cell communication and microenvironmental signaling responses. CCN2 is known to be overexpressed in several cardiovascular diseases, but its role is not completely understood. Methods: Here, CCN2 involvement in aortic wall homeostasis and response to vascular injury was investigated in inducible Ccn2 -deficient mice, with induction of vascular damage by infusion of Ang II (angiotensin II; 15 days), which is known to upregulate CCN2 expression in the aorta. Results: Ang II infusion in CCN2-silenced mice lead to 60% mortality within 10 days due to rapid development and rupture of aortic aneurysms, as evidenced by magnetic resonance imaging, echography, and histological examination. Ccn2 deletion decreased systolic blood pressure and caused aortic structural and functional changes, including elastin layer disruption, smooth muscle cell alterations, augmented distensibility, and increased metalloproteinase activity, which were aggravated by Ang II administration. Gene ontology analysis of RNA sequencing data identified aldosterone biosynthesis as one of the most enriched terms in CCN2-deficient aortas. Consistently, treatment with the mineralocorticoid receptor antagonist spironolactone before and during Ang II infusion reduced aneurysm formation and mortality, underscoring the importance of the aldosterone pathway in Ang II–induced aorta pathology. Conclusions: CCN2 is critically involved in the functional and structural homeostasis of the aorta and in maintenance of its integrity under Ang II–induced stress, at least, in part, by disruption of the aldosterone pathway. Thus, this study opens new avenues to future studies in disorders associated to vascular pathologies.

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Section: Discussionmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 96%

CCN2 (Cellular Communication Network Factor 2) Deletion Alters Vascular Integrity and Function Predisposing to Aneurysm Formation

et al. 2022

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“…In addition, during the past decade, several potential diagnosis-predictive markers, such as high sensitivity C-reactive protein (hs-CRP) [ 27 – 29 ], D- dimer (DD) [ 30 – 33 ], serum amyloid A (SAA) [ 34 ], relaxin 2 (RL2) [ 35 ], have been reported. However, those markers were lack of specificity though they have some features for the clinical preliminary assessment and the markers themself have some factors suffering disturbance.…”

Section: Discussionmentioning

confidence: 99%

Assessing serum levels of SM22α as a new biomarker for patients with aortic aneurysm/dissection

Zhang

Wang

et al. 2022

PLoS ONE

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Background Aortic aneurysm/dissection (AAD) is now encountered more often because of the increasing prevalence of atherosclerosis and hypertension in the population. Despite many therapeutic improvements, in particular timely and successful surgery, in-hospital mortality rates are still higher. Timely identification of patients at high risk will help improve the overall prognosis of AAD. Since early clinical and radiological signs are nonspecific, there is an urgent need for accurate biomarkers. Smooth muscle 22α (SM22α) is a potential marker for AAD because of its abundant expression in vascular smooth muscle, which is involved in development of AAD. Methods We prepared three different mouse models, including abdominal aortic aneurysm, neointimal hyperplasia and atherosclerosis. SM22α levels were assessed in serum and vascular tissue of the mice. Next, the relationships between serum SM22α level and vascular lesion were studied in mice. Finally, serum from 41 patients with AAD, 107 carotid artery stenosis (CAS) patients and 40 healthy volunteers were tested for SM22α. Serum levels of SM22α were measured using an enzyme-linked immunosorbent assay (ELISA). Results Compared with the controls, serum SM22α levels were reduced in the models of aortic aneurysm, neointimal formation and atherosclerosis, and elevated in mice with ruptured aneurysm. Serum SM22α level was negatively correlated with apoptosis rate of vascular smooth muscle cells (VSMC), ratio of intima/ media (I/M) area and plaque size. Patients with AAD had significantly higher serum SM22α levels than patients with only CAS, or normal controls. Conclusion Serum SM22α could be a potential predictive marker for AAD, and regulation of VSMC is a possible mechanism for the effects of SM22α.

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“…In addition, Yuchen et al reported significantly high levels of SSA in patients with AAD than in healthy controls. Thus, SSA was an independent prognostic factor in patients with AAD during hospitalization [ 23 ]. This study suggested that patients with elevated NPR had a worse long-term prognosis; the two-factor survival analysis showed that a high NPR had a certain prognostic value in different types and treatment methods.…”

Section: Discussionmentioning

confidence: 99%

High Neutrophil-to-Platelet Ratio Is Associated with Poor Survival in Patients with Acute Aortic Dissection

et al. 2022

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Background. Acute aortic dissection (AAD), a serious and fatal cardiovascular disease, is characterized by inflammation that may further aggravate the condition. We evaluated the value of the neutrophil-to-platelet ratio (NPR) in the prognosis of AAD. Methods. We collected records of patients with AAD and clinical data from 2010 to 2020 and followed up on the relevant information for 136 months. The Kaplan–Meier (K–M) survival along with the univariate and multivariate Cox analyses was used to examine the prognostic value of NPR in AAD. In addition, nomograms were constructed by combining NPR, age, Stanford typing, and treatment methods. The accuracy of nomograms was evaluated using calibration plots, and the prediction efficiency of nomograms was evaluated by receiver operating characteristic curve analysis and decision curve analysis (DCA). Results. The K–M analysis showed that AAD patients with higher NPR exhibited worse prognosis. In addition, different Stanford typing and treatment methods produced varied prognosis results. Univariate and multivariate Cox analyses showed that NPR value, age, classification, and treatment were independent prognostic factors for the overall survival time of patients with AAD. Nomograms constructed by combining NPR, age, Stanford typing, and treatment methods showed good predictive efficacy, and the AUC values for 1-, 3-, and 5-year predicting were 0.82, 0.79, and 0.74, respectively. Conclusions. Our results suggest that pretreatment NPR can be used as a potential prognostic marker of overall survival time in patients with AAD.

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Serum amyloid a protein as a potential biomarker in predicting acute onset and association with in-hospital death in acute aortic dissection

Cited by 14 publications

References 34 publications

CCN2 (Cellular Communication Network Factor 2) Deletion Alters Vascular Integrity and Function Predisposing to Aneurysm Formation

CCN2 (Cellular Communication Network Factor 2) Deletion Alters Vascular Integrity and Function Predisposing to Aneurysm Formation

Assessing serum levels of SM22α as a new biomarker for patients with aortic aneurysm/dissection

High Neutrophil-to-Platelet Ratio Is Associated with Poor Survival in Patients with Acute Aortic Dissection

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