Identification of Lysophosphatidylcholines and Sphingolipids as Potential Biomarkers for Acute Aortic Dissection via Serum Metabolomics

Zhou, Xiaoxu; Wang, Renping; Zhang, Tian; Liu, Fei; Zhang, Wei; Wang, Guili; Gu, Guorong; Han, Qinqi; Xu, Da; Yao, Chenling; Guo, Daqiao; Fu, Weiguo; Qi, Yunpeng; Wang, Lixin

doi:10.1016/j.ejvs.2018.07.004

Cited by 47 publications

(34 citation statements)

References 32 publications

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“…Our study showed that the AAD patients have elevated mean systolic pressure, leukocyte count and D-dimer level. These results are slightly different from the previous results [ 33 , 34 ]. The increased mean systolic pressure may be related to decompensation for myocardial ischemia in the patients, while the increased leukocyte count might result from inflammation due to the tear of vascular intima.…”

Section: Discussioncontrasting

confidence: 99%

Clinical features and risk factors of postoperative in-hospital mortality following surgical repair of Stanford type A acute aortic dissection

Chen

et al. 2021

BMC Cardiovasc Disord

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Background To investigate the clinical features of patients with Stanford type A acute aortic dissection (AAD) and analyze the risk factors affecting postoperative in-hospital mortality rate. Methods The demographic and clinical data were retrospectively collected and analyzed from 118 AAD patients admitted to the Affiliated Hospital of Hangzhou Normal University from June 2016 to April 2019. All patients underwent surgical treatment and were grouped into death and survival groups. The risk factors affecting postoperative in-hospital death were analyzed using multivariate logistic regression analysis. Results The male to female ratio in the patients was 3.8:1 and the mean age was 50.11 ± 9.91 years. The patient’s main comorbidities were hypertension (70.33%) and coronary heart disease (10.17%). The main symptoms included chest pain and back pain (72.89%). The highest incidence of complications was pericardial effusion (48.31%), followed by pleural effusion (22.88%). The mean systolic blood pressure, white blood cell count and D-dimer in the patients were over the ranges of normal people. The incidences of cardiac and renal insufficiency were 18.64% and 16.95% respectively, and the postoperative in-hospital mortality rate was 12.71%. Univariable analysis showed that age, renal insufficiency, cardiac insufficiency, D-dimer level, cardiopulmonary bypass time, operation time, blood transfusion volume and postoperative hemostasis were significant factors leading to the death (P < 0.05). Multivariate logistic regression analysis showed that age > 65, renal insufficiency, cardiopulmonary bypass time ≥ 250 min and postoperative hemostasis were independent risk factors for the death (P < 0.05). Conclusions AAD patients frequently have underlying diseases with pain as the main symptom. Age > 65 years, renal insufficiency, cardiopulmonary bypass time ≥ 250 min and postoperative hemostasis are significantly risk factors for postoperative mortality.

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Section: Discussioncontrasting

confidence: 99%

Clinical features and risk factors of postoperative in-hospital mortality following surgical repair of Stanford type A acute aortic dissection

Chen

et al. 2021

BMC Cardiovasc Disord

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“…We used Biocrates AbsoluteIDQ ® p180 kit (Innsbruck, Austria), which does not enable separation of isomers of lipids; thus, for deeper understanding of the role of complex lipids in AAA pathogenesis we need further separate, well-focused, and standardized lipidomics studies [ 22 ]. Recently, it was also reported that sphingolipids and LysoPCs were significantly reduced in patients with acute aortic dissection [ 23 ]. An active sphingomyelinase-ceramide pathway, characterized by increased levels of ceramides and metabolisation of sphingomyelins (e.g., by oxidized LDL-induced sphingomyelinase activity), leads to reduced levels of sphingomyelins [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Metabolomic Profile of Abdominal Aortic Aneurysm

et al. 2021

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Abdominal aortic aneurysm (AAA) is characterized by structural deterioration of the aortic wall, leading to aortic dilation and rupture. The aim was to compare 183 low molecular weight metabolites in AAA patients and aorta-healthy controls and to explore if low molecular weight metabolites are linked to AAA growth. Blood samples were collected from male AAA patients with fast (mean 3.3 mm/year; range 1.3–9.4 mm/year; n = 39) and slow growth (0.2 mm/year; range −2.6–1.1 mm/year; n = 40), and from controls with non-aneurysmal aortas (n = 79). Targeted analysis of 183 metabolites in plasma was performed with AbsoluteIDQ p180 kit. The samples were measured on a QTRAP 4500 coupled to an Agilent 1260 series HPLC. The levels of only four amino acids (histidine, asparagine, leucine, isoleucine) and four phosphatidylcholines (PC.ae.C34.3, PC.aa.C34.2, PC.ae.C38.0, lysoPC.a.C18.2) were found to be significantly lower (p < 0.05) after adjustment for confounders among the AAA patients compared with the controls. There were no differences in the metabolites distinguishing the AAA patients with slow or fast growth from the controls, or distinguishing the patients with slow growth from those with fast growth. The current study describes novel significant alterations in amino acids and phosphatidylcholines metabolism associated with AAA occurrence, but no associations were found with AAA growth rate.

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“…Rheumatoid arthritis is related to increased LPC expression that is positively correlated with cardiovascular risks ( Giraud et al, 2019 ). Moreover, LPC and sphingolipids showed significant expression alteration in patients with acute aortic dissection and are suggested to be used as potential biomarkers for its diagnosis ( Zhou et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

The Inhibitory Effect of Lysophosphatidylcholine on Proangiogenesis of Human CD34+ Cells Derived Endothelial Progenitor Cells

Zhao

2021

Front. Mol. Biosci.

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Increasing evidence reveals that lysophosphatidylcholine (LPC) is closely related to endothelial dysfunction. The present study aimed to investigate the mechanism of LPC in inhibiting the proangiogenesis and vascular inflammation of human endothelial progenitor cells (EPCs) derived from CD34+ cells. The early EPCs were derived from CD34+ hematopoietic stem cells whose purity was identified using flow cytometry analysis. The surface markers (CD34, KDR, CD31; VE-cadherin, vWF, eNOS) of EPCs were examined by flow cytometry analysis and immunofluorescence. RT-qPCR was used to detect the mRNA expression of inflammatory cytokines (CCL2, IL-8, CCL4) and genes associated with angiogenesis (VEGF, ANG-1, ANG-2) in early EPCs after treatment of LPC (10 μg/ml) or phosphatidylcholine (PC, 10 μg/ml, control). The angiogenesis of human umbilical vein endothelial cells (HUVECs) incubated with the supernatants of early EPCs was detected by a tube formation assay. The mRNA and protein levels of key factors on the PKC pathway (phosphorylated PKC, TGF-β1) were measured by RT-qPCR and western blot. The localization of PKC-β1 in EPCs was determined by immunofluorescence staining. We found that LPC suppressed the expression of CCL2, CCL4, ANG-1, ANG-2, promoted IL-8 expression and had no significant effects on VEGF expression in EPCs. EPCs promoted the angiogenesis of HUVECs, which was significantly inhibited by LPC treatment. Moreover, LPC was demonstrated to promote the activation of the PKC signaling pathway in EPCs. In conclusion, LPC inhibits proangiogenesis of human endothelial progenitor cells derived from CD34+ hematopoietic stem cells.

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Identification of Lysophosphatidylcholines and Sphingolipids as Potential Biomarkers for Acute Aortic Dissection via Serum Metabolomics

Cited by 47 publications

References 32 publications

Clinical features and risk factors of postoperative in-hospital mortality following surgical repair of Stanford type A acute aortic dissection

Clinical features and risk factors of postoperative in-hospital mortality following surgical repair of Stanford type A acute aortic dissection

Metabolomic Profile of Abdominal Aortic Aneurysm

The Inhibitory Effect of Lysophosphatidylcholine on Proangiogenesis of Human CD34+ Cells Derived Endothelial Progenitor Cells

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