Occurrence Of Abdominal Aortic Aneurysm Research Articles

The Role of Inflammasome in Abdominal Aortic Aneurysm and Its Potential Drugs.

Abdominal aortic aneurysm (AAA) has been recognized as a serious chronic inflammatory degenerative aortic disease in recent years. At present, there is no other effective intervention except surgical treatment for AAA. With the aging of the human population, its incidence is increasing year by year, posing a serious threat to human health. Modern studies suggest that vascular chronic inflammatory response is the core process in AAA occurrence and development. Inflammasome, a multiprotein complex located in the cytoplasm, mediates the expression of various inflammatory cytokines like interleukin (IL)-1β and IL-18, and thus plays a pivotal role in inflammation regulation. Therefore, inflammasome may exert a crucial influence on the progression of AAA. This article reviews some mechanism studies to investigate the role of inflammasome in AAA and then summarizes several potential drugs targeting inflammasome for the treatment of AAA, aiming to provide new ideas for the clinical prevention and treatment of AAA beyond surgical methods.

The occurrence and development of abdominal aortic aneurysm may be related to the energy metabolism disorder and local inflammation

BackgroundThe cellular mechanism of the formation of abdominal aortic aneurysm (AAA) is very complicated. A series of sophisticated events eventually led to significant pathological changes in the anatomical structure and function of the arterial wall and they are still not clear nowadays. MethodsWe pooled publicly available GEO datasets (GSE57691 and GSE47472) to get a comprehensive comparisons between normal tissues and AAA tissues to try to reveal molecular mechanism underlying the disease. Total 63 AAA samples and 18 normal tissue samples were compared and we fond that there were 784 significantly different gene (DEGs, threshold set as adjusted P < 0.05 and Log FC < 1) were identified. At the same time, we validate the possible signaling factor expression of AAA by comparing the normal tissue of the human body with the AAA tissue. ResultsIn the pathway enrichment, we found that FOXP3 related signaling pathways, inflammation-related cytokine signaling pathways, interleukin-8-CXCR1 related signaling pathways and VEGFA and FGFR1 related signal pathway were significantly enrichmented. In Weighted gene co-expression network analysis (WGCNA), we found that the key hub genes were significantly related to lipid catabolic metabolism, which further verified the possibility that AAA might relate to energy metabolism disorders. ConclusionBased on the comprehensive analysis of previous high-throughput data and the validation of basic experiments, we found that the occurrence of AAA may be related to energy metabolism disorders and local inflammation.

Ganglioside GM3 Protects Against Abdominal Aortic Aneurysm by Suppressing Ferroptosis.

Abdominal aortic aneurysm (AAA) is a potentially life-threatening vascular condition, but approved medical therapies to prevent AAA progression and rupture are currently lacking. Sphingolipid metabolism disorders are associated with the occurrence and development of AAA. It has been discovered that ganglioside GM3, a sialic acid-containing type of glycosphingolipid, plays a protective role in atherosclerosis, which is an important risk factor for AAA; however, the potential contribution of GM3 to AAA development has not been investigated. We performed a metabolomics study to evaluated GM3 level in plasma of human patients with AAA. We profiled GM3 synthase (ST3GAL5) expression in the mouse model of aneurysm and human AAA tissues through Western blotting and immunofluorescence staining. RNA sequencing, affinity purification and mass spectrometry, proteomic analysis, surface plasmon resonance analysis, and functional studies were used to dissect the molecular mechanism of GM3-regulating ferroptosis. We conditionally deleted and overexpressed St3gal5 in smooth muscle cells (SMCs) in vivo to investigate its role in AAA. We found significantly reduced plasma levels of GM3 in human patients with AAA. GM3 content and ST3GAL5 expression were decreased in abdominal aortic vascular SMCs in patients with AAA and an AAA mouse model. RNA sequencing analysis showed that ST3GAL5 silencing in human aortic SMCs induced ferroptosis. We showed that GM3 interacted directly with the extracellular domain of TFR1 (transferrin receptor 1), a cell membrane protein critical for cellular iron uptake, and disrupted its interaction with holo-transferrin. SMC-specific St3gal5 knockout exacerbated iron accumulation at lesion sites and significantly promoted AAA development in mice, whereas GM3 supplementation suppressed lipid peroxidation, reduced iron deposition in aortic vascular SMCs, and markedly decreased AAA incidence. Together, these results suggest that GM3 dysregulation promotes ferroptosis of vascular SMCs in AAA. Furthermore, GM3 may constitute a new therapeutic target for AAA.

Brucella-infected abdominal aortic aneurysm: management strategies for an uncommon aneurysm.

The occurrence of Brucella-induced abdominal aortic aneurysms is an exceedingly rare phenomenon, yet it stands as one of the most severe complications within this context. The combined utilization of serological testing and imaging diagnostics has been validated as an effective approach for the identification of Brucella-induced abdominal aortic aneurysms. Presently, the predominant therapeutic strategies encompass antibiotic treatment and surgical intervention. Nonetheless, ongoing controversies persist concerning the establishment of diagnostic criteria, the optimal timing and selection of antibiotic regimens, and the nuanced decision between open surgical procedures and endovascular interventions. Through a meticulous analysis of cases originating from our institution as well as a comprehensive review of previously documented instances, we aim to engage in a detailed discourse on the salient diagnostic and therapeutic facets surrounding Brucella-induced abdominal aortic aneurysms. We conducted a retrospective summary of three cases involving Brucella-induced abdominal aortic aneurysms treated within our institution. Furthermore, we performed a comprehensive PubMed search, without imposing restrictions on language or publication year, to identify pertinent literature pertaining to Brucella-induced abdominal aortic aneurysms. The selection criteria primarily focused on case reports delineating occurrences of abdominal aortic aneurysms attributed to Brucella infection. We present three distinct cases of Brucella-induced abdominal aortic aneurysms managed at our institution, providing comprehensive insights into the employed diagnostic and therapeutic approaches. Additionally, over the past five decades, a total of 24 cases in 23 publications of Brucella-induced abdominal aortic aneurysms have been reported on PubMed. The earliest report dates back to 1976. Our analysis suggests that Brucella-induced abdominal aortic aneurysm is characterized by a remarkably low incidence but is associated with a substantial risk of life-threatening complications. The integration of serological and imaging assessments assumes pivotal importance in facilitating prompt diagnosis of this condition. The prompt initiation of targeted antibiotic therapy is recommended, and the selection of appropriate surgical strategies should be guided by considerations including aneurysm dimensions and morphological attributes. The timely identification and intervention carry utmost significance in retarding disease advancement and ameliorating unfavorable clinical outcomes.

Transcription Factor TCF3 Promotes Macrophage-Mediated Inflammation and MMP Secretion in Abdominal Aortic Aneurysm by Regulating miR-143-5p /CCL20.

Damage to the abdominal aortic wall and the local inflammatory response are key factors resulting in abdominal aortic aneurysm (AAA) formation. During this process, macrophage polarization plays a key role. However, in AAA, the regulatory mechanism of macrophages is still unclear, and further research is needed. In this study, we found that the transcription factor TCF3 was expressed at low levels in AAA. We overexpressed TCF3 and found that TCF3 could inhibit MMP and inflammatory factor expression and promote M2 macrophage polarization, thereby inhibiting the progression of AAA. Knocking down TCF3 could promote M1 polarization and MMP and inflammatory factor expression. In addition, we found that TCF3 increased miR-143-5p expression through transcriptional activation of miR-143-5p , which further inhibited expression of the downstream chemokine CCL20 and promoted M2 macrophage polarization. Our research indicates that TCF3-mediated macrophage polarization plays a key regulatory role in AAA, complementing the role and mechanism of macrophages in the occurrence and development of AAA and providing a scientific basis for AAA treatment.

Status of diagnosis and therapy of abdominal aortic aneurysms.

Abdominal aortic aneurysms (AAAs) are characterized by localized dilation of the abdominal aorta. They are associated with several serious consequences, including compression of adjacent abdominal organs, pain, treatment-related financial expenditure. The main complication of AAA is aortic rupture, which is responsible for about 200,000 deaths per year worldwide. An increasing number of researchers are dedicating their efforts to study AAA, resulting in significant progress in this field. Despite the commendable progress made thus far, there remains a lack of established methods to effectively decelerate the dilation of aneurysms. Therefore, further studies are imperative to expand our understanding and enhance our knowledge concerning AAAs. Although numerous factors are known to be associated with the occurrence and progression of AAA, the exact pathway of development remains unclear. While asymptomatic at most times, AAA features a highly unpredictable disease course, which could culminate in the highly deadly rupture of the aneurysmal aorta. Current guidelines recommend watchful waiting and lifestyle adjustment for smaller, slow-growing aneurysms, while elective/prophylactic surgical repairs including open repair and endovascular aneurysm repair are recommended for larger aneurysms that have grown beyond certain thresholds (55 mm for males and 50 mm for females). The latter is a minimally invasive procedure and is widely believed to be suited for patients with a poor general condition. However, several concerns have recently been raised regarding the postoperative complications and possible loss of associated survival benefits on it. In this review, we aimed to highlight the current status of diagnosis and treatment of AAA by an in-depth analysis of the findings from literatures.

Identification of core cuprotosis-correlated biomarkers in abdominal aortic aneurysm immune microenvironment based on bioinformatics.

The occurrence of abdominal aortic aneurysms (AAAs) is related to the disorder of immune microenvironment. Cuprotosis was reported to influence the immune microenvironment. The objective of this study is to identify cuprotosis-related genes involved in the pathogenesis and progression of AAA. Differentially expressed lncRNAs (DElncRNAs) and mRNAs (DEmRNAs) in mouse were identified following AAA through high-throughput RNA sequencing. The enrichment analyses of pathway were selected through Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG). The validation of cuprotosis-related genes was conducted through immunofluorescence and western blot analyses. Totally, 27616 lncRNAs and 2189 mRNAs were observed to be differentially expressed (|Fold Change| ≥ 2 and q< 0.05) after AAA, including 10424 up-regulated and 17192 down-regulated lncRNAs, 1904 up-regulated and 285 down-regulated mRNAs. Gene ontology and KEGG pathway analysis showed that the DElncRNAs and DEmRNAs were implicated in many different biological processes and pathways. Furthermore, Cuprotosis-related genes (NLRP3, FDX1) were upregulated in the AAA samples compared with the normal one. Cuprotosis-related genes (NLRP3,FDX1) involved in AAA immune environment might be critical for providing new insight into identification of potential targets for AAA therapy.

Identification of Novel Biomarkers for Abdominal Aortic Aneurysm Promoted by Obstructive Sleep Apnea

We sought to find new biomarkers for abdominal aortic aneurysms (AAA) caused by chronic intermittent hypoxia (CIH). The AAA mice model was created using Ang II. The mice were divided into normoxic and CIH groups. The structure of AAA was observed using abdominal ultrasonography, Elastica van Gieson (EVG), and hematoxylin and eosin (HE) staining. The expression of ɑ-SMA was investigated using immunohistochemistry. The novel biomarkers were screened using bioinformatics analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to verify the expression of novel genes in both normal oxygen and CIH. CIH appears to cause greater aortic dilation, higher AAA incidence, lower survival rate, thicker vessel wall, and more brittle elastic lamellae when compared to controls. The immunohistochemistry results showed that the expression of ɑ-SMA in the CIH group was reduced significantly. Four novel genes, including Homer2, Robo2, Ehf, and Asic1, were found to be differentially expressed between normal oxygen and CIH using qRT-PCR, indicating the same trend as bioinformatics analysis. We discovered that CIH could hasten the occurrence and progression of AAA. Four genes (Homer2, Robo2, Ehf, and Asic1) may be novel biomarkers for AAA, which could aid in the search for new therapies for patients with AAA caused by CIH.

Abdominal Aortic Aneurysms: Epidemiological, Clinical and Echographic Aspects in The Health Structures of Lomé and At The Kara University Hospital (TOGO)

Objective To describe the epidemiological, clinical and arterial Doppler ultrasound aspects of abdominal aortic aneurysm (AAA). Material and methods This is a prospective study with descriptive and analytical aims carried out from January 2019 to March 2022 (3 years) at the cardiovascular exploration center (CEC) "Saint-Esprit" of the association of the people's doctors for the research on cardiovascular diseases (AMP-MCV), at the clinic "Le Printemps" and at the University Hospital of Kara. All patients who underwent arterial Doppler ultrasound of the lower limbs for any reason in these centers during the study period were included. Ultrasound scans were performed or confirmed by a physician with a diploma specializing in vascular Doppler ultrasound. Results We retained 32 Doppler ultrasound scans out of 739 performed for AAA with a frequency of 4.38%. The mean age was 73.5± 9.07 years. The sex ratio M/F was 1.4. The cardiovascular medical history (84.38%) found was: hypertension (33.33%), diabetes (18.52%), dyslipidemia (33.33%) and a combination of diabetes and hypertension (14.81%). The circumstances of discovery were: downstream MI ischemia (72%), incidental finding on abdominal ultrasound (15.63%) and De bakey sign (6.25%). The location of the aneurysms was subrenal (84.4%), suprarenal (9.4%) and both (6.2%). AAAs were fusiform (71.9%) and saccular (28.1%). The size of the aneurysms was greater than 5 cm in 78.17% of patients. High blood pressure increases the probability of the occurrence of subrenal AAA while dyslipidemia increases the occurrence of fusiform AAA. Diabetes increases the probability of occurrence of AAA larger than 7cm. AAAs were thrombosed in 75% of patients. There were extensions of the aneurysms to the iliac arteries in 70.59%. Downstream embolic complications represented 46.88%, in the form of occlusions and tight stenoses. Spontaneous mortality was 81.24%. Conclusion Arterial Doppler ultrasonography is a very important tool in the screening, positive and lesion diagnosis of AAA. The risk factors for AAA are: age over 60 years, male gender, hypertension, diabetes and dyslipidemia. Early detection remains essential, because the spontaneous prognosis is poor.

Regular medication as a risk factor for intracranial aneurysms: A comparative case-control study.

Previous medical history strongly contributes to the genesis of intracranial aneurysms (IA). A possible impact of regular medication on the occurrence of abdominal aortic aneurysms has been reported. To evaluate the value of regular medication on the risk of development and rupture of IA. Data on medication use and related comorbidities were obtained from the institutional IA registry. A 1:1 age- and sex-matched patient sample was collected from the population-based Heinz Nixdorf Recall Study with individuals from the same area. In the analysis comparing IA cohort (n = 1960) with the matched normal population (n = 1960), the use of statins (adjusted odds ratio, 1.34 [95% confidence interval 1.02-1.78]), antidiabetics (1.46 [1.08-1.99]), and calcium channel blockers (1.49 [1.11-2.00]) was independently associated with higher risk of IA, whereas uricostatics (0.23 [0.14-0.38]), aspirin (0.23 [0.13-0.43]), beta-blockers (0.51 [0.40-0.66]), and angiotensin-converting enzyme inhibitors (0.38 [0.27-0.53]) were related to lower risk of IA. In the multivariable analysis within the IA cohort (n = 2446), SAH patients showed higher drug exposure with thiazide diuretics (2.11 [1.59-2.80]), but lower prevalence of remaining antihypertensive medication-beta-blockers (0.38 [0.30-0.48]), calcium channel blockers (0.63 [0.48-0.83]), angiotensin-converting enzyme inhibitors (0.56 [0.44-0.72]), and angiotensin-1 receptor blockers (0.33 [0.24-0.45]). Patients with ruptured IA were less likely to be treated with statins (0.62 [0.47-0.81]), thyroid hormones (0.62 [0.48-0.79]), and aspirin (0.55 [0.41-0.75]). Regular medication might impact the risks related to the development and rupture of IA. Further clinical trials are required to clarify the effect of regular medication on IA genesis.

Overexpressed DDX3x promotes abdominal aortic aneurysm formation and activates AKT in ApoE knockout mice

In recent years, abdominal aortic aneurysm (AAA) lesions have become one of the important diseases that threaten public health. Related studies have confirmed that the occurrence of abdominal aortic aneurysms is related to inflammatory stress, cell apoptosis, and elastic fiber degradation. DDX3x is thought to interact with inflammasomes such as NLRP3 to aggravate the process of the inflammatory response, but its role in the occurrence of AAA remains unclear. Since DDX3x is indispensable in animal embryonic growth, we used an adeno-associated virus to construct gene-overexpressing mice to induce aneurysm development through AngII infusion. The results indicated that the incidence of aneurysms, inflammatory cell infiltration, vascular smooth muscle cell transformation, and oxidative stress levels were significantly increased under the condition of DDX3x overexpression. At the signaling level, activation of the AKT pathway exacerbates aneurysm formation. Taken together, we believe that DDX3x plays a key role in the development of aneurysms and may be a new target for the treatment of aneurysm progression.

MiR-124a Involves in the Regulation of Wnt/β-Catenin and P53 Pathways to Inhibit Abdominal Aortic Aneurysm via Targeting BRD4.

Background Abdominal aortic aneurysm (AAA) belongs to a progressive, gradual aortic rupture, which can lead to death without surgical intervention. The key factors regulating the occurrence and progress of AAA are not clear. Increasing studies have indicated that microRNA (miRNA) plays an important role in cancer development. miR-124a serves as a tumor suppressor in several neoplasms, and its upregulation can greatly inhibit the life activities such as malignant growth and migration of tumor cells. Aim The objective of this study is to explore the association of miR-124a with AAA and to uncover the regulated mechanism of miR-124a on AAA progression. Methods The specimens from the AAA patients were used for observing the miR-124a expression, and human aortic endothelial cells (hAoECs) were treated with AngII to establish the AAA cell models. The quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR), CCK-8, transwell assay, flow cytometry assay, and western blot were conducted to unearth the regulation mechanism of miR-124a on AAA, and the dual-luciferase reporter assay was employed to investigate the downstream target of miR-124a. Results miR-124a was significantly downregulated in the whole blood of the patients, and the decreased miR-124a was also observed in AAA cell models. Overexpressing miR-124a could effectively inhibit the proliferation and migration and promote the apoptosis of the AAA cells. The dual-luciferase reporter assay confirmed that BRD4 was a downstream target of miR-124a, and BRD4 upregulation could obviously reverse the effects of miR-124a on the phenotype of AAA cells. Moreover, it was found that miR-124a could regulate the activities of Wnt/β-catenin and P53 pathways via targeting the BRD4. Conclusion Our data suggested that miR-124a could regulate the activities of Wnt/β-catenin and P53 to suppress the AAA progression via targeting the BRD4.

Sequential Minimally Invasive Treatment of Concomitant Abdominal Aortic Aneurysm and Colorectal Cancer: A Single-Center Experience

The surgical management of concomitant occurrence of abdominal aortic aneurysm (AAA) and colorectal cancer (CRC) is still controversial. Conversely, benefits from a minimally invasive approach are well known concerning the treatment of both AAA and CRC. The aim of this study is to assess safety and feasibility of a sequential 2-staged minimally invasive during the same recovery by endovascular aneurysm repair (EVAR) technique and laparoscopic colorectal resection. From January 2008 to December 2020, all patients with concomitant AAA and CRC were consecutively treated by EVAR and laparoscopic colorectal resection. Perioperative data were retrospectively collected in order to evaluate short- and long-term outcomes following the sequential 2-staged procedures. A total of 24 patients were included. The localization of the aneurysm was infrarenal abdominal aortic in 23 cases and in one case of common iliac artery. EVAR procedure has always been performed first. In 18 patients, a percutaneous access has been used while in 6 patients a surgical access has been adopted. Twelve patients had cancer in the left colon, 9 in the right colon, and 3 patients had rectal cancer. No conversions or intraoperative complications had occurred during laparoscopic surgery. The major complications rate after EVAR and CRC surgery was 8.3% and 12.5%, respectively. The mean interval between EVAR and CRC treatment was 7.8 ± 1 and the mean length of stay was 15.4 ± 3.6. No deaths occurred during hospitalization and between the procedures. Overall mortality was 20.8% with a mean follow-up of 39.41 ± 19.2 months. Elective sequential 2-staged minimally invasive treatment is a safe and feasible approach with acceptable morbidity and mortality rates and it should be adopted in current clinical practice to manage concomitant AAA and CRC.

Metabolomic Profile of Abdominal Aortic Aneurysm

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.

Potency of miR-144-3p in promoting abdominal aortic aneurysm progression in mice correlates with apoptosis of smooth muscle cells

Abdominal aortic aneurysm (AAA), a life-threatening disease, is commonly diagnosed among people with risk factors, including increasing age, male gender, and smoking. The apoptosis of smooth muscle cells (SMCs) has been reported to disrupt the vascular structural integrity, which causes AAA. Thus, we sought to characterize the potential role of microRNA (miR)-144-3p in SMC apoptosis, and to outline the molecular mechanisms involved in this pathway. We collected pathological abdominal aortic tissues and adjacent normal aortic biopsy specimens from 18 patients undergoing AAA repair surgery. The relationship between miR-144-3p expression and SMC proliferation was assessed by transfecting mimic/inhibitor of miR-144-3p in human aortic smooth muscle cells (HASMCs). Anti-growth effect of miR-144-3p and related genes was evaluated in a murine AAA model. Dual luciferase reporter gene assay was adopted to validate the targeting relationship between miR-144-3p and enhancer of zeste homolog 2 (EZH2), and the enrichment of EZH2 in the p21 promoter region was determined by chromatin immunoprecipitation assay. MiR-144-3p was highly expressed in AAA tissues. Enhanced miR-144-3p diminished SMC proliferation by binding to the EZH2 3′-untranslated region and thereby inhibiting EZH2 expression. In addition, EZH2 was highly enriched in the promoter region of p21, and knockdown of p21 expression could rescue the effect of miR-144-3p on SMC proliferation and apoptosis. miR-144-3p serves as a promoter for the apoptosis of SMCs, which contributes to the occurrence and progression of AAA. This observation will serve as the basis for further investigations into potential p21-based therapies for AAA treatment.

The potential role of plasma fibroblast growth factor 21 as a diagnostic biomarker for abdominal aortic aneurysm presence and development

AimsFibroblast growth factor 21 (FGF21) has been identified as the master hormonal regulator of energy balance, its elevation is observed in a series of metabolic and cardiovascular diseases. Studies have implicated the role of FGF21 signaling in the pathogenesis of abdominal aortic aneurysm (AAA). We will investigate the association of FGF21 and AAA development. Materials and methodsIn this study, we assayed plasma levels of FGF21 in 82 patients with AAA and 44 control subjects, then analyzed their relationship with clinical, biochemical and histological phenotypes. The expression of β-klotho, an essential co-receptor of FGF21, was assessed with IHC staining and RT-qPCR. Machine learning models incorporate a combination of FGF21 and clinical data were utilized in the prediction of AAA occurrence. Key findingsFGF21 was statistically higher in patients with AAA (781 pg/ml [533, 1213]) than in control subjects (567 pg/ml [324, 939]). After adjustment for age and BMI, we found a positive association of FGF21 levels with AAA diameters, hypertension rate and hsCRP, and a negative correlation between FGF21 levels and HDL-c. Furthermore, the protein levels of β-klotho in abdominal aorta of AAA were found significantly lower than in control group indicating the presence of FGF21 resistance. Combining FGF21 levels with four clinical characteristics significantly improved the stratification of AAA and control groups with an AUC of 0.778. SignificanceCombining detection of plasma FGF21 and clinical characteristics may be reliable for identifying the presence of AAA. The role of FGF21 as a therapeutic target of AAA warrants further investigation.

Advanced Research of Abdominal Aortic Aneurysms on Metabolism

Abdominal aortic aneurysm (AAA) is a cardiovascular disease with a high risk of death, seriously threatening the life and health of people. The specific pathogenesis of AAA is still not fully understood. In recent years, researchers have found that amino acid, lipid, and carbohydrate metabolism disorders play important roles in the occurrence and development of AAA. This review is aimed to summarize the latest research progress of the relationship between AAA progression and body metabolism. The body metabolism is closely related to the occurrence and development of AAA. It is necessary to further investigate the pathogenesis of AAA from the perspective of metabolism to provide theoretical basis for AAA diagnosis and drug development.

Polymorphisms in the IL-6 and TNF-α gene are associated with an increased risk of abdominal aortic aneurysm

BackgroundAn abdominal aortic aneurysm (AAA) is a complex disease of the aging population that is associated with inflammation and the cellular immune response. To investigate the influence of interleukin (IL)-6 and tumor necrosis factor (TNF)-α single nucleotide polymorphisms (SNPs) on the risk of AAA formation and progression, the frequency of AAA and its associated risk factors were determined. MethodFour SNPs in the IL-6 (−174G/C, rs1800795; −572G/C, rs1800796) and TNF-α (−238G/A, rs361525; −308G/A, rs1800629) genes were studied by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in patients with AAA and healthy volunteers. The mRNA expression and plasma IL-6 and TNF-α levels were also determined. ResultsA mutation detected in at least one allele of the IL-6 -174G/C SNP was associated with a 2-fold increased risk of AAA occurrence (OR: 2.08; 95% CI: 1.15–3.76; p = 0.014, in the dominant model). An increased risk of AAA incidence among heterozygous carriers of the TNF-α − 308G/A genotype was observed (OR: 2.06; 95% CI: 1.17–3.62; p = 0.011, in the overdominant model). The wild-type genotypes of the IL-6 -174G/C and the TNF-α -308G/A SNPs coexisted more frequently in healthy subjects than in AAA patients and was associated with decreased risk of AAA (p < 0.001). Moreover, elevated levels of IL-6 and TNF-α were associated with an increased risk of hypertension (p < 0.001 and p = 0.022, respectively). ConclusionsThe IL-6 -174G/C and the TNF-α -238G/A gene polymorphisms are associated with an increased risk of abdominal aortic aneurysm development.

The Role of Serum Calprotectin as a New Marker in Abdominal Aortic Aneurysms - A Preliminary Report.

Abdominal Aortic Aneurysm (AAA) remains a surgical challenge. There are many recognizable markers associated with the formation of AAA. Previous experiments carried out on animal models have shown a correlation between serum calprotectin and the occurrence of AAA. This study aimed to evaluate the level of calprotectin as a potential diagnostic biomarker in patients with diagnosed AAA. The study group consisted of 75 patients aged 35-75 years assigned to two groups: a control group (n=43) of healthy subjects without AAA and a study group (n=32) of patients with a diagnosed AAA. The first calprotectin test was performed upon patient admission to the hospital, and the second control test was performed after three months. The concentration of calprotectin in plasma was determined using the Immunoenzymatic Method (ELISA) with the commercially available Assaypro Kit (AssayMax™ Human Calprotectin ELISA Kit), as well as the sandwich method with polyclonal antibodies to human calprotectin and peroxidase enzyme. Serum calprotectin levels in AAA patients were three times higher than in healthy subjects (p<0.05). A statistically significant twofold decrease in calprotectin concentration was observed after AAA surgery compared to the control group (p<0.05). Calprotectin levels can be an important marker in the detection of AAA. In conclusion, AAA patients showed a threefold increase in serum calprotectin level and a twofold decrease in this marker after AAA surgery.

TLR2 2029C/T and TLR3 1377C/T and -7C/A Polymorphisms Are Associated with the Occurrence of Abdominal Aortic Aneurysm.

TLRs are a family of signaling sensors that play a crucial role in the host immune response and are involved in the modulation of inflammatory processes. To study their contribution to abdominal aortic aneurysm (AAA) formation and development, we determined the frequency of TLR2, TLR3, TLR4, and TLR9 single-nucleotide polymorphisms (SNPs) and investigated the association between polymorphisms and the risk of AAA incidence. A total of 104 patients with AAAs and 112 healthy, unrelated volunteers were screened for the presence of TLR2 (2029C/T and 2258G/A), TLR3 (1377C/T, 1234C/T, and -7C/A), TLR4 (896A/G, 1196C/T, and 3266G/A), and TLR9 (-1237T/C, -1486T/C, 1174G/A, and 2848C/T) SNPs by using PCR-RFLP analysis. The heterozygous genotype of the TLR2 2029C/T SNP was more common in patients with AAA than in healthy subjects (p < 0.0001) and was associated with at least an 8-fold increased risk of AAA incidence (p < 0.001). The wild-type genotype of the TLR3 -7C/A SNP was associated with a 3-fold increased risk of hypertension (p = 0.026). The heterozygous TLR3 genotype 1377C/T and -7C/A SNPs were less common in patients with AAA than in healthy subjects (p < 0.0001 and p = 0.0004, respectively) and were associated with a decreased risk of AAA occurrence (p < 0.001 and p = 0.0012, respectively). No relation to AAA risk was found for TLR4 SNPs. Heterozygous genotypes of the TLR2 2029C/T and TLR3 1377C/T and -7C/A SNPs may serve as genetic biomarkers of AAA incidence.