Macrophages are a key heterogeneous cell population involved in the pathogenesis and progression of acute aortic dissection (AD), though their mechanisms remain unclear. This study aims to identify the gene driving inflammatory damage in acute AD within a specific macrophage subcluster, highlighting potential therapeutic targets. Single-cell RNA sequencing (scRNA-seq) was employed to analyze the cellular heterogeneity in acute AD and normal aortic tissues. Bioinformatic analysis was conducted to identify the key gene. The role of sphingosine kinase 1 (SPHK1) was further explored using human acute AD tissue samples, macrophage cell line experiments, and AD mouse models. scRNA-seq identified six macrophage subclusters in AD tissues, with subcluster a exhibiting a pronounced pro-inflammatory phenotype. SPHK1 was significantly upregulated in this subcluster and was identified as the key regulatory gene. In vitro, inhibition of SPHK1 reduced macrophage-mediated inflammatory damage via the S1P-S1PR2/3-RhoA-ROCK1 signaling pathway. In vivo studies revealed a 40

Abdominal aortic aneurysm (AAA) is a common vascular disease among the elderly with considerable mortality risk. Current therapeutic strategies, such as open surgical repair and endovascular repair, primarily reduce rupture risk by mechanically excluding the aneurysm but have limited effects on the underlying inflammation and structural deterioration of the aortic wall. Nanomaterials, with their tunable structures and microenvironment-responsive properties, offer new opportunities for precise intervention and vascular reconstruction. This review focuses on the pathological microenvironment of AAA, detailing key processes such as inflammatory and immune imbalance, extracellular matrix degradation, protease network activation, and oxidative stress, and maps out potential therapeutic targets. It summarizes advances in polymer-based, inorganic, and biomimetic nanoplatforms for drug delivery, targeting proteases and reactive oxygen species, local anti-inflammatory and immunomodulation, as well as mechanical reinforcement and tissue repair using biomimetic extracellular matrix nanofibers, hydrogels, or stent nanocoatings. The value and limitations of ultrasmall superparamagnetic iron oxide contrast agents and theranostic nanoplatforms for imaging-based assessment and monitoring are also discussed. Two technical pathways are highlighted: lesion-microenvironment-guided targeted nanotherapy and intelligent vascular repair through microenvironment remodeling. The review emphasizes shifting treatment goals from merely controlling aneurysm expansion to restoring arterial wall structure and function, while acknowledging ongoing challenges in safety evaluation, scalable manufacturing, and clinical integration. Overall, pathological microenvironment-based nanotheranostic strategies show promising potential to modulate disease progression, promote vascular repair, improve risk assessment, and enable more individualized long-term management of AAA.

Objective: This study aimed to assess whether patients with hostile aortic neck (HAN) anatomy achieve comparable outcomes to those with standard aortic neck (SAN) following endovascular aneurysm repair (EVAR). Additionally, developed and externally validated an anatomical risk score model based on the entire cohort to guide access-prepared neck embolization for intraoperative type Ia endoleak (IaEL). Methods: A multicenter retrospective cohort study was conducted in two phases. Phase I compared baseline characteristics, intraoperative endoleaks, and strategies, as well as technical and clinical success between groups. Phase II identified independent anatomical predictors using multivariate logistic regression and developed a score model to facilitate intraoperative IaEL risk stratification for preoperative planning. Results: A total of 326 patients were included. The overall technical success rate was 98.2%, with no significant difference between groups ( P = 1.000). HAN cases had longer procedure times (85.0 vs. 71.0 min; P < 0.001). The overall survival (86.6% ± 6.7% vs 88.4% ± 5.8%; mean ± standard error), freedom from reintervention (92.8% ± 2.7% vs 91.9% ± 2.6%), and clinical success (91.5% ± 2.8% vs 90.9% ± 2.7%) were comparable between patients with HAN and those with SAN over 48 months (all P > 0.05). Intraoperative IaEL occurred more often in HAN (37.1% vs 2.5%, P < 0.001). Neck length, infrarenal angulation, and conical neck were assigned weighted points to construct a six-point scoring system for intraoperative IaEL. The score model demonstrated robust discrimination (AUC = 0.853 in training and 0.842 in validation) and may serve as a tool for intraoperative risk stratification and procedural planning. Conclusions: EVAR in HAN patients can achieve outcomes comparable to those in SAN patients when intraoperative procedures are performed. The risk score offers a practical tool for preoperative risk stratification and anatomy-based procedural planning.

The male gender has traditionally been considered a potential risk factor for vascular diseases, especially given the gender disparity in many degenerative vascular conditions. This has led to the hypothesis that androgens may be detrimental, while estrogen confers vascular protection. However, this perspective overlooks the gradual decline in androgen levels in men after middle age, despite the increasing incidence of vascular diseases. Numerous studies have demonstrated an association between lower testosterone levels and higher rates of vascular disease and mortality, challenging the conventional view. Although the exact mechanisms remain unclear, growing evidence suggests that physiological levels of androgens play a protective role in vascular physiology and pathophysiology. This review consolidates findings on these conflicting roles, proposing that under normal conditions, androgen levels exert protective effects, while adverse outcomes are more likely in scenarios such as supraphysiological testosterone exposure or specific clinical settings, like testosterone replacement therapy, where risks continue to be debated. A more nuanced understanding of this dual role is critical for guiding future research and therapeutic approaches.

Treating renal cell carcinoma (RCC) is clinically challenging because the characteristic hypoxic microenvironment of RCC serves as a key driver of malignant progression. High-throughput sequencing analysis across multiple models was used in this study to identify PLOD3 as a major oncogene driving RCC development. PLOD3 promoted RCC cell growth and metastatic capacity in vivo and in vitro. Mechanistically, HIF-2α and histone lactylation modification jointly upregulate PLOD3 expression levels. PLOD3 specifically binds to the C2 domain of NEDD4, hindering NEDD4 autoinhibition and triggering NEDD4 to activate E3 ubiquitin ligase function. This process affects GOT2 expression via inducing K48-linked ubiquitination, leading to GOT2 degradation via the ubiquitin-proteasome pathway. Thus, PLOD3 participates in reprogramming glutamine metabolism through influencing the stability GOT2 protein. This study establishes PLOD3 as a key oncogenic driver of RCC, with HIF-2α/PLOD3/NEDD4/GOT2 pathway potentially being a therapeutic target and providing biomarkers for treating RCC.

Efferocytosis plays a crucial role in maintaining the stability of the immune microenvironment. Increasing research indicates that efferocytosis core genes (ECGs) are not only widely expressed in immune cells, but also expressed at significant levels in tumour cells, impacting tumour progression. However, the comprehensive effects of ECGs on cancer prognosis and the immune microenvironment remain underexplored. This study analysed data from 33 tumour types to assess the expression, diagnostic and prognostic values of ECGs as well as gene modification landscapes. It also predicted the correlation between ECGs, the immune microenvironment and responses to immunotherapy, revealing that lower ECGs expression levels were associated with better immunotherapy responses in various cancers. Additionally, molecular docking studies simulated the interactions between TIMD4 and its sensitive drugs, facilitating targeted drug development. Finally, both in vitro and in vivo experiments confirmed that silencing TIMD4 could effectively inhibit the proliferation and invasion of renal cell carcinoma. Overall, TIMD4 can be used as an important biomarker for tumour prognosis and immunotherapy response, providing new insights into the mechanisms of tumour immune microenvironment and progression, as well as a novel therapeutic target.

Obesity is a significant risk factor for cardiovascular diseases. Although previous studies have shown uncertainty about its role in aortic dissection (AD), our clinical observations showed that most younger patients with acute AD have a significantly higher body mass index. The underlying reasons are yet to be investigated. Recent studies have suggested that obesity is linked to vascular pathophysiology, including endothelial injury, medial remodeling and deficiency, perivascular adipose tissue dysfunction, and systemic dysfunction. Understanding the association between obesity and acute AD can aid in recognizing high-risk populations, providing an earlier chance of diagnosis and intervention, and improving clinical outcomes for acute AD in young obese patients. This review analyzes and integrates current data to explain the potential role of obesity in acute AD pathogenesis.

Background Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, with therapeutic resistance posing a significant clinical challenge. Metabolic reprogramming, a hallmark of cancer, enables tumor cells to alter metabolic pathways to meet their increased energy and biosynthetic demands, playing a critical role in HCC initiation, progression, and drug resistance. Aim of Review This review aims to elucidate the mechanisms underlying metabolic alterations in HCC, including fatty acid, protein, and amino acid metabolism, and to explore their implications in tumor progression and therapeutic resistance. Additionally, it highlights emerging therapeutic strategies targeting key enzymes in metabolic pathways for HCC. Key Scientific Concepts of Review Metabolism reprogramming is closely associated with HCC proliferation and metastasis, while the interplay between metabolic pathways further drives disease progression. Targeting key metabolic enzymes and pathways through combination therapies and novel drug development shows promising clinical potential. This review provides a comprehensive analysis of metabolic reprogramming in HCC and underscores the importance of understanding these mechanisms to develop more effective therapeutic interventions.

BACKGROUND:Abdominal aortic aneurysm (AAA) is a severe aortic disease for which no pharmacological interventions have yet been developed. This investigation focused on identifying protein-based therapeutic targets and assessing how proteins mediate the interplay between modifiable risk factors and AAA development. METHODS:Causal inferences between plasma proteins and AAA were drawn using 2-sample Mendelian randomization, followed by comprehensive sensitivity testing, colocalization, and replication efforts. Further analyses included database interrogation, single-cell RNA data analysis, enrichment analysis, protein-protein interaction networks, and immunohistochemistry to map the tissue-specific expression of these proteins, their expression within AAA tissues, and their biological roles. Mediation Mendelian randomization was employed to evaluate the mediating effects of AAA-related proteins on the associations between AAA and 3 risk factors: hypertension, smoking, and obesity. RESULTS:A total of 43 proteins were identified as having causal links to AAA. Colocalization analysis pinpointed 13 proteins with strong evidence of colocalization with AAA. Of these, the causal involvement of 10 proteins was substantiated by external validation data. Consistent evidence for PCSK9 (proprotein convertase subtilisin/kexin type 9), IL6R (interleukin-6R), ECM1 (extracellular matrix protein 1), and ANGPTL4 (angiopoietin-related protein 4) was further validated through tissue immunohistochemistry and blood data. Moreover, Mendelian randomization analysis identified 10 proteins as mediators of the influence of hypertension, smoking, and obesity on AAA development. CONCLUSIONS:This analysis identifies 4 proteins (PCSK9, IL6R, ECM1, and ANGPTL4) as high-priority therapeutic targets for AAA and emphasizes the intermediary role of plasma proteins in linking hypertension, smoking, obesity, and AAA. Further investigations are needed to clarify the specific roles of these proteins in AAA pathology.

BACKGROUND:Besides anticoagulation as the main conservative treatment for primary aortic mural thrombus (PAMT), whether further aggressive intervention of primary aortic lesion should be performed remains controversial. METHODS:PubMed, Ovid, and SAGE databases were systematically searched to identify studies on the management of PAMT using anticoagulation alone or/and treatment of aorta published between 2000 and 2022. RESULTS:Ninety-nine studies, total 250 patients, were included in this study. They were into 2 groups: conservative treatment group (137 patients) and aortic treatment group (113 patients). There was no significant difference in the basic characteristics between the 2 groups. In both groups, peripheral embolisms complicated by PAMT were firstly managed by medical therapy, intervention, or surgery. Then, for PAMT, conservative treatment group received only medical treatment (mainly anticoagulation) continuously, while aortic treatment group also received further aggressive intervention. Patients in the aortic treatment group showed a lower rate of overall complications (22.1% vs. 47.4%), lower recurrence rate of aortic thrombus (5.3% vs. 35.8%), and lower recurrence rate of peripheral embolism (4.4% vs. 30.7%). Complications of conservative group include various forms of bleeding, recurrence of aortic thrombus, and recurrent peripheral embolism. A small number of patients died of critical condition, and most complications were managed by endovascular treatment or surgery. Patients with aortic treatment were further divided into open surgery group (72 patients) and endovascular therapy group (41 patients), and endovascular therapy showed lower overall complications risk than open surgery (4.9% vs. 31.9%). CONCLUSION:Although anticoagulation is a basic and major conservative treatment for PAMT, a further early aggressive aortic management may lead to a lower recurrence of aortic thrombus, lower recurrence of peripheral embolic events, and less complication despite risks.

Abdominal aortic aneurysm (AAA) is a life-threatening condition characterized by the dilation of the abdominal aorta, leading to a high risk of rupture. Current treatment options are limited, particularly for patients ineligible for surgical interventions. This study explores a novel immunotherapeutic approach using chimeric antigen receptor Treg cells targeting vascular cell adhesion molecule-1 (VCAM-1) to mitigate AAA progression. By leveraging the specificity and regulatory function of CAR-Treg cells, our research aims to modulate the immune response and reduce inflammation in the aneurysmal wall. Results from preclinical mouse models demonstrated that CAR-Treg cells effectively homed to the aneurysmal site, suppressed local inflammation, and decreased aortic dilation compared to control groups. These findings suggest that CAR-Treg cell therapy could provide a promising, non-surgical treatment option for AAA patients, addressing a critical unmet need in cardiovascular disease management.

OBJECTIVE:To evaluate the association between computed tomography angiography (CTA)-derived plaque features and composition and ipsilateral embolic stroke of undetermined source (ESUS) in patients with nonstenotic (<50%) extracranial carotid atherosclerosis. METHODS:Patients with acute neurological symptoms who underwent head and neck CTA between May 2021 and May 2024 were retrospectively enrolled. Those with nonstenotic extracranial carotid plaques were included, comprising individuals with anterior circulation ESUS and controls without ESUS. Plaque morphology and compositional profiles were assessed. RESULTS:A total of 161 carotid arteries were analyzed, including 70 ipsilateral to an ESUS and 91 from controls. Morphological features of nonstenotic carotid plaques differed significantly between the ESUS and control groups. Plaque subcomponent volumes were quantified by using 3D Slicer software and the relative proportions of lipid, fibrous, and calcified components differed significantly between groups. Multivariate analysis identified internal carotid artery and common carotid artery diameters, positive remodeling, and a smaller calcification volume percentage as independent predictors of ESUS (odds ratio [OR], 8.37 [P = .015]; OR, 4.50 [P < .001]; OR, 0.23 [P = .008]). A nomogram incorporating these factors demonstrated predictive utility for ESUS risk. CONCLUSIONS:CTA-derived characteristics of nonstenotic carotid plaques effectively identified plaque features associated with ESUS. Larger internal carotid artery and common carotid artery diameters, positive remodeling, and reduced calcification volume percentage were independent predictors of high-risk plaques. These findings can refine risk stratification and help to guide individualized therapeutic strategies.

During endovascular total aortic arch repair by in situ fenestration, extra procedures are needed to sustain cerebral blood flow when targeting all three supra-aortic branches. Recently, our group has successfully interposed a chimney balloon between greater curvature of aortic arch and an aortic stent to safeguard cerebral blood flow during total endovascular aortic arch repair.

Rupture of advanced carotid atherosclerotic plaques increases the risk of ischaemic stroke, which has significant global morbidity and mortality rates. However, the specific characteristics of immune cells with dysregulated function and proven biomarkers for the diagnosis of atherosclerotic plaque progression remain poorly characterised. Our study elucidated the role of immune cells and explored diagnostic biomarkers in advanced plaque progression using single-cell RNA sequencing and high-dimensional weighted gene co-expression network analysis. We identified a subcluster of monocytes with significantly increased infiltration in the advanced plaques. Based on the monocyte signature and machine-learning approaches, we accurately distinguished advanced plaques from early plaques, with an area under the curve (AUC) of 0.899 in independent external testing. Using microenvironment cell populations (MCP) counter and non-negative matrix factorisation, we determined the association between monocyte signatures and immune cell infiltration as well as the heterogeneity of the patient. Finally, we constructed a convolutional neural network deep learning model based on gene-immune correlation, which achieved an AUC of 0.933, a sensitivity of 92.3%, and a specificity of 87.5% in independent external testing for diagnosing advanced plaques. Our findings on unique subpopulations of monocytes that contribute to carotid plaque progression are crucial for the development of diagnostic tools for clinical diseases.

C-C chemokine ligand 5 (CCL5) plays a crucial role in the advancement of human cancer. Nevertheless, little is known about the multi-omics characterisation of CCL5 and its significance for the immune microenvironment and prognosis of tumor patients. The basal expression levels of the CCL5 gene in normal human tissues, aberrant expression in disease, genomic alterations, prognostic roles, pathway enrichment, immune microenvironment, association with immune checkpoints, drug sensitivity, and the ability to predict patients’ immunotherapeutic response to immune checkpoint inhibitors (ICIs) and small molecule drugs were all thoroughly analyzed using data gathered from 33 cancers. Lastly, we were able to validate CCL5’s involvement in renal clear cell carcinoma by experimental means. We discovered that CCL5 has distinct expression patterns and a diagnostic biomarker significance in cancer. Furthermore, we discovered that CCL5 is essential for both the tumor microenvironment and pan-cancer. TMB and MSI are two frequent immunological checkpoints that are significantly correlated with CCL5, and patients who express high levels of CCL5 have stronger immunotherapeutic response and a better prognosis after immunotherapy. Eventually, molecular docking was used to find small molecule inhibitors that can specifically target CCL5. Ultimately, it was shown that CCL5 knockdown impeded renal clear cell carcinoma cells’ ability to proliferate and invade. Our findings demonstrate the significant potential of CCL5 as an immunotherapeutic response biomarker and prognostic indicator, which may pave the way for more studies on the mechanism of tumor infiltration and CCL5’s potential therapeutic applications in cancer.

ObjectiveThe aim of this study was to investigate whether intimal arterial calcification (IAC) and medial arterial calcification (MAC) are correlated with the various clinical outcomes following endovascular therapy (EVT) for peripheral arterial disease (PAD).MethodsThis single-center retrospective study comprised 154 consecutively hospitalized individuals with PAD who underwent EVT for de novo femoral-popliteal calcific lesions from January 2016 to July 2021. The predominant calcification patterns of IAC and MAC were assessed using a semi-quantitative computed tomography scoring system. The Kaplan-Meier method and Cox regression were conducted to evaluate the correlations between calcification patterns and medium- to long-term outcomes.ResultsThe distribution of calcification patterns was as follows: IAC in 111 patients (72%) and MAC in 43 patients (28%). No remarkable variation was noted between the IAC and MAC groups regarding age (P = .84) and gender (P = .23). The MAC group indicated lower rates of 4-year primary patency, assisted primary patency, secondary patency, and amputation-free survival (AFS) compared with the IAC group (24% ± 7% vs 40% ± 6%; P = .003; 30% ± 8% vs 51% ± 6%; P = .001; 51% ± 8% vs 65% ± 5%; P = .004; and 43% ± 9% vs 76% ± 5%; P < .001, respectively). There was no significant difference in the rate of freedom from clinically driven target lesion revascularization between the MAC and IAC groups (63% ± 10% vs 73% ± 5%; P = .26). Stepwise multivariable Cox regression analysis demonstrated that MAC was associated with poor patency (hazard ratio, 1.81; 95% confidence interval, 1.12-2.93; P = .016) and AFS (hazard ratio, 2.80; 95% confidence interval, 1.52-5.16; P = .001).ConclusionsCompared with IAC, MAC is independently associated with lower medium- to long-term patency and AFS after EVT for de novo femoral-popliteal occlusive lesions.

Senescence-induced therapy was previously considered as an effective treatment for tumors, and cellular senescence was initially regarded as an effective mechanism against cancer. However, whether cell senescence-related genes can be used to predict the prognosis of papillary thyroid carcinoma (PTC) and immunotherapy remains unclear. We developed and validated a cell senescence-related signature (CSRS) by analyzing the gene expression of 278 genes related to cellular senescence in 738 patients with PTC. Additionally, further analysis showed that CSRS was a reliable predictor of patient outcomes in combination with immune checkpoint expression and drug susceptibility, and patients with high risk scores may benefit from immunotherapy. The findings of this study demonstrate that CSRS serves as an immunotherapeutic response and prognosis biomarker affecting the tumor immune microenvironment of PTC.

The T cell marker CD6 regulates both T cells and target cells during inflammatory responses by interacting with its receptors. However, only a few receptors binding to the extracellular domains of CD6 have been identified, and cellular events induced by CD6 engagement with its receptors in target cells remain poorly understood. In this study, we identified CD44 as a novel CD6 receptor by proximity labeling and confirmed the new CD6-CD44 interaction by biochemical and biophysical approaches. CD44 and the other 2 known CD6 receptors, CD166 and CDCP1, were distributed diffusely on resting retinal pigment epithelium (RPE) cells but clustered together to form a receptor complex upon CD6 binding. CD6 stimulation induced dramatic remodeling of the actomyosin cytoskeleton in RPE cells mediated by activation of RhoA, and Rho-associated kinase signaling, resulting in increased myosin II phosphorylation. Such actomyosin activation triggered the disassembly of tight junctions responsible for RPE barrier integrity in a process that required all components of the tripartite CD6 receptor complex. These data provided new insights into the mechanisms by which CD6 mediates T cell-driven disruption of tissue barriers during inflammation. CD44 is a new receptor of CD6 and CD6 interacts with all 3 identified receptors to regulate cytoskeleton redmodeling.

dCTP pyrophosphatase 1 (DCTPP1) is widely expressed in tumors and the immune system and plays a critical role in human cancer progression. However, multi-omics characterization of DCTPP1 and its role in prognosis and immune microenvironment of tumor patients has not been explored. We collected data from 33 cancers and comprehensively analyzed the aberrant expression, prognostic role, pathway enrichment, immune microenvironment, and association with drug sensitivity of DCTPP1 in cancers, as well as the prediction of patients’ immunotherapeutic response to ICIs and targeted small molecule drugs. Finally, we experimentally confirmed the role of DCTPP1 in renal clear cell carcinoma. We discovered that DCTPP1 has a differentiable expression and a diagnostic biomarker significance in cancer. Additionally, we discovered that DCTPP1 is important for the tumor microenvironment and pan-cancer. TMB and MSI are frequent immunological checkpoints that are significantly correlated with DCTPP1 expression. Patients who express high levels of DCTPP1 have greater rates of survival and therapeutic response following immunotherapy. Ultimately, it was discovered that renal clear cell carcinoma cells’ invasion and proliferation were suppressed by DCTPP1 knockdown. Our findings demonstrate the significant potential of DCTPP1 as a biomarker for prognosis and immunotherapeutic response, which may pave the way for more investigation into the mechanism of tumor infiltration and DCTPP1’s potential for cancer therapy.

Objective Despite surgical advance, effective targeted drugs for non-surgical treatment of abdominal aortic aneurysm (AAA) are lacking because of the unclear pathogenesis of AAA. N6-methyladenosine (m6A) methylation, acknowledged for its pivotal influence on RNA metabolism, including aspects such as stability, transport, translation, and splicing, is largely implied for its role in AAA mechanism. This study aims to elucidate the involvement of m6A methylation in the progression of AAA through an integrative multi-omics and machine learning approach.Methods and Results We utilized methylated RNA immunoprecipitation sequencing (MeRIP-seq) to map the m6A methylation landscape in AAA tissues and combined this with RNA sequencing (RNA-seq) from the GEO database, to explore the interplay between m6A methylation and gene expression. A machine learning-based AAA m6A-related mRNA signature (AMRMS) was developed to predict the risk of AAA dilation. The AMRMS showed robust predictive power in distinguishing between patients with large and small AAAs. Notably, FKBP11 was identified as a key gene significantly influencing the predictive model, and up-regulated in large AAAs compared to its in small AAAs. Further single-cell RNA sequencing (scRNA-seq) and histological analysis highlighted the critical role of FKBP11 in mediating the endoplasmic reticulum stress of plasma cells within the AAA walls and its correlation with m6A methylation.Conclusions The m6A modification regulatory network plays a vital role in the progression of AAA, and the AMRMS offers promising potential in assessing the risk of AAA dilation. Our findings suggest that elevated FKBP11, by activating endoplasmic reticulum stress in plasma cells, may significantly contribute to AAA expansion.### Competing Interest StatementThe authors have declared no competing interest.* AAA : abdominal aortic aneurysm AMRMS : AAA m6A-related mRNA signature AUC : Area Under the Curve BP : biological process CBBs : Cell Barcoded Magnetic Beads CC : cellular component CCA : Canonical Correlation Analysis CMUaB : CMU Aneurysm Biobank CDS : coding sequence CTA : computed tomography angiography DEGs : differential expressed genes DMGs : differentially methylated genes ECs : endothelial cells Enet : Elastic Network ER : endoplasmic reticulum FC : Fold Change GBM : Generalized Boosted Regression Modeling glmBoost : Generalized Linear Model Boosting GO : gene ontology HC : healthy control IHC : Immunohistochemistry IP : immunoprecipitation KEGG : Kyoto encyclopedia of genes and genomes LDA : Linear Discriminant Analysis LOOCV : Leave-One-Out Cross-Validation m6A : N6-methyladenosine MASS : Multicenter Aneurysm Screening Study MeRIP-seq : methylated RNA immunoprecipitation with next-generation sequencing MF : molecular function MPs : mononuclear phagocytes NKCs/TCs : natural killer cells/T cells PCs : plasma cells PCA : principal Component Analysis PPI : Protein-Protein Interactions RF : Random Forest ROC : Receiver Operating Characteristic SMCs : smooth muscle cells SMGs : specific methylated genes Stepglm : Step Generalized Linear Model SVM : Support Vector Machine t-SNE : t-Distributed Stochastic Neighbor Embedding Teff : Effector T cells Th : Helper T cells Treg : Regulatory T cells UMI : unique molecular identifiers UPR : unfolded protein response XGBoost : eXtreme Gradient Boosting 3’UTR : 3’ untranslated region 5’UTR : 5’ untranslated region.