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Aortic Aneurysm: Mechanisms, Biomarkers, and Therapeutic Strategy
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Aortic Aneurysm: Mechanisms, Biomarkers, and Therapeutic Strategy

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 October 2026 | Viewed by 5128

Editors

Dr. Mitra Esfandiarei

E-Mail Website
Guest Editor
1. Biomedical Sciences Program, College of Graduate Studies, Midwestern University, Glendale, AZ 85308, USA
2. College of Medicine Phoenix, University of Arizona, Phoenix, AZ 85004, USA
Interests: vascular biology; aneurysms; endothelial function; angiotensin signaling; genetic aortic diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Seda Selamet Tierney

E-Mail Website
Guest Editor
Vascular Research Laboratory, Stanford Medicine Heart Center, Division of Cardiology, Stanford University, Stanford, CA 94305, USA
Interests: pediatric cardiology; aortic aneurysm; echocardiography; Marfan syndrome; Kawasaki disease

Special Issue Information

Dear Colleagues,

Aortic aneurysm remains a life-threatening vascular disease that can lead to high morbidity and mortality, despite significant progress in diagnostic imaging, surgical techniques, and pharmacological interventions. The complexity of its pathogenesis—encompassing genetic predisposition, inflammatory processes, extracellular matrix remodeling, endothelial dysfunction, and altered smooth muscle cell signaling—necessitates multidisciplinary investigation to uncover novel mechanisms and therapeutic strategies.

This Special Issue of Biomedicines, titled “Aortic Aneurysm: Mechanisms, Biomarkers, and Therapeutic Strategy”, aims to showcase cutting-edge basic, translational, and clinical research that advances our understanding of the molecular, cellular, and biomechanical underpinnings of aortic aneurysm. In addition, it will highlight innovations in diagnosis, risk stratification, and therapeutics. We welcome contributions from diverse fields, including vascular biology, genetics, molecular medicine, biomechanics, pharmacology, and surgery. We emphasize the importance of an integrative approach to this complex disease utilizing in vitro, ex vivo, and in vivo experimental models.

Topics of interest include, but are not limited to, the following: 

  • Molecular and cellular mechanisms driving aortic aneurysm initiation and progression;
  • Role of smooth muscle cells, endothelial cells, and immune cells in aneurysm pathology;
  • Genetic and epigenetic determinants of syndromic and non-syndromic aneurysms;
  • Sex differences and hormonal influences on aneurysm development and rupture risk;
  • Oxidative stress, nitric oxide signaling, and vascular inflammation;
  • Advanced imaging techniques and biomarkers for early detection and risk assessment;
  • Biomechanical modeling and wall stress analysis in aneurysm growth and rupture prediction;
  • Experimental pharmacological approaches and repurposing of existing drugs;
  • Crosstalk between aortic aneurysm and systemic metabolic or cardiovascular disorders;
  • Insights from animal models, organ-on-chip, and tissue-engineered vascular models;
  • Translational studies using animal models;
  • Clinical trials of novel interventions.

This Special Issue strives to convene a global community of researchers and clinicians dedicated to unraveling the complexities of aortic aneurysm disease and paving the way toward innovative, patient-centered care. We cordially invite you to contribute your latest findings and insights to this Special Issue and help shape the future of aortic aneurysm research and treatment.

Dr. Mitra Esfandiarei
Dr. Seda Selamet Tierney
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • aortic aneurysms
  • genetic aortic diseases
  • endothelial dysfunction
  • extracellular matrix
  • aortic wall
  • aortic smooth muscle
  • angiotensin system
  • aortic wall elasticity
  • matrix metalloproteinases

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Published Papers (6 papers)

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Research

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11 pages, 462 KB  
Article
Women with Abdominal Aortic Aneurysms Have a Different Pattern of Genetic Variability, Compared to Men
by Jonas Wallinder, Anders Wanhainen, Helena Åkerud, Dick Wågsäter and Martin Björck
Biomedicines 2026, 14(5), 1172; https://doi.org/10.3390/biomedicines14051172 - 21 May 2026
Viewed by 550
Abstract
Background/Objectives: The etiology behind sex differences in the prevalence of abdominal aortic aneurysm (AAA) can only partly be explained by environmental factors such as smoking. Genetic factors are also likely to be part of the explanation since family history is common. We hypothesized [...] Read more.
Background/Objectives: The etiology behind sex differences in the prevalence of abdominal aortic aneurysm (AAA) can only partly be explained by environmental factors such as smoking. Genetic factors are also likely to be part of the explanation since family history is common. We hypothesized that genetic factors on AAA prevalence might be different between the sexes. Methods: This study is designed as a case–control study with 83 female AAA patients, 101 female controls, 97 male AAA patients, and 196 male controls. Single nucleotide polymorphism (SNP) analysis was performed comparing 13 different SNPs. The selection of SNPs was based on previous SNP association studies, estrogen receptors, and SNPs important to inflammation and lipid metabolism, as these processes are modulated by estrogen. Results: A multivariable logistic regression resulted in significant differences in SNP association with AAA development between men and women in two SNPs (rs2010963 and rs8113877). Significant differences were found between cases and controls, using univariate analysis, in four SNPs: rs8113877 among women, and in rs6511720, rs2010963 and rs4988300 among men. No SNPs were significantly different compared to controls in both men and women. SNP rs8113877 is located in the promotor of the MMP-9 gene. Levels of circulating MMP-9 were measured in a subgroup of the study participants: an association between MMP-9 and AAA was found, and the association between rs8113877 and MMP-9 was sex-dependent. Conclusions: Genetic variability associated with AAA differs between men and women; these differences should be accounted for in future research. Full article
(This article belongs to the Special Issue Aortic Aneurysm: Mechanisms, Biomarkers, and Therapeutic Strategy)
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13 pages, 1905 KB  
Article
Semaglutide Prevents Aortic Rupture and Dissection in the Angiotensin II Mouse Model
by Amanda Balboa Ramilo, Kevin Mani, Anders Wanhainen, Henrik Lodén, Anna Nilsson, Per E. Andrén, Malou Friederich-Persson and Dick Wågsäter
Biomedicines 2026, 14(4), 933; https://doi.org/10.3390/biomedicines14040933 - 20 Apr 2026
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Abstract
Background and aims: Abdominal aortic aneurysm (AAA) is a vascular disease characterized by the progressive dilation of the aorta, culminating in rupture. At present, there are no pharmacological treatments to prevent AAA development or reduce rupture rate. A recent study showed that patients [...] Read more.
Background and aims: Abdominal aortic aneurysm (AAA) is a vascular disease characterized by the progressive dilation of the aorta, culminating in rupture. At present, there are no pharmacological treatments to prevent AAA development or reduce rupture rate. A recent study showed that patients prescribed Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have significantly lower risks of mortality, AAA repair, and acute abdominal aortic syndrome. Semaglutide is a GLP-1RA with increased agonist capacity and longer half-life, compared to earlier generations of GLP-1RAs. In this study, we aimed to investigate the role and mechanisms of semaglutide in the prevention of AAA development and rupture in a murine model. Methods: AAA was induced in apolipoprotein-E-deficient mice, by continuous subcutaneous infusion of angiotensin II. Treatment with semaglutide (12 µg/kg) began seven days after disease induction (rescue trial) or simultaneously with disease induction (prophylactic trial). At experimental endpoint, aortic diameter was measured by high-frequency ultrasound and the aortic tissue was collected for histological analysis. Results: Prophylactic treatment with semaglutide drastically reduced mortality by dissection and rupture during the first seven days of disease development, but did not affect AAA formation at 28 days. Histological evaluation of the aorta at day seven showed a normal vessel wall thickness with a trend for a higher content of collagen in the aortic wall in mice treated with semaglutide, compared to controls. Conclusions: Semaglutide prevents aortic rupture and dissection in the early phases of AAA development in the angiotensin II mouse model, likely by promoting the maintenance of an adequate proportion of collagen in the vessel wall. Full article
(This article belongs to the Special Issue Aortic Aneurysm: Mechanisms, Biomarkers, and Therapeutic Strategy)
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13 pages, 1621 KB  
Article
Mitochondrial Functional Capacity Is Impaired in Angiotensin II-Infused Mice and Not Recovered by Metformin
by Amanda Balboa Ramilo, Kevin Mani, Anders Wanhainen, Malou Friederich-Persson and Dick Wågsäter
Biomedicines 2026, 14(4), 759; https://doi.org/10.3390/biomedicines14040759 - 26 Mar 2026
Viewed by 719
Abstract
Background: The pathophysiological mechanisms of Abdominal Aortic Aneurysm (AAA) are not elucidated. Alterations in mitochondrial function, such as a reduction in oxidative phosphorylation (OXPHOS), have been observed at genome level and functionally in vascular smooth muscle cells. Metformin reduces AAA development and growth [...] Read more.
Background: The pathophysiological mechanisms of Abdominal Aortic Aneurysm (AAA) are not elucidated. Alterations in mitochondrial function, such as a reduction in oxidative phosphorylation (OXPHOS), have been observed at genome level and functionally in vascular smooth muscle cells. Metformin reduces AAA development and growth in diabetic patients, but the precise mechanisms are not known. In this paper we aim to demonstrate the feasibility of measuring mitochondrial functional capacity ex vivo in intact murine aneurysmal tissue and confirm a decrease in OXPHOS, and to determine if the protective effect of metformin on AAA is mediated by mitochondrial function. Methods: AAA was induced in ApoE KO mice by administration of angII (1000 ng/kg/min) through osmotic minipumps. Metformin was administered in drinking water at a dose of 100 mg/kg/day. The abdominal aorta was isolated in situ and mitochondrial functional capacity was analyzed ex vivo in whole permeabilized tissue by high-resolution respirometry. Results: Mitochondrial respiration was successfully measured ex vivo in whole aneurysmal tissue. Mitochondrial function was impaired in angII-treated mice, with decreased fold change in Complex I and Complex I+II oxygen consumption, relative to basal levels. Complex II oxygen consumption was also decreased in angII-treated mice. Rescue treatment of mice with metformin did not affect or restore mitochondrial function. Conclusions: Mitochondrial function can be evaluated in murine whole aneurysmal tissue, providing a method for a physiological approach to the study of mitochondrial function in AAA. Mitochondrial function is impaired in AAA. However, rescue treatment with metformin is not sufficient to recover mitochondrial function and seems not to be the mechanism behind prevention of aneurysm. Full article
(This article belongs to the Special Issue Aortic Aneurysm: Mechanisms, Biomarkers, and Therapeutic Strategy)
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21 pages, 3040 KB  
Article
The Metabolite Differences in Vascular Smooth Muscle Cells of Abdominal Aortic Aneurysm Revealed by Untargeted Metabolomics
by Yuqi Yi, Ke Hu, Yuxuan Li, Jie Li and Hongping Deng
Biomedicines 2026, 14(3), 623; https://doi.org/10.3390/biomedicines14030623 - 11 Mar 2026
Cited by 3 | Viewed by 1007
Abstract
Background: Abdominal aortic aneurysm (AAA) is a vascular disease with a high mortality rate upon rupture (85–90%). Surgical repair remains the most effective intervention, whereas pharmacological treatments to prevent aneurysm expansion or rupture are limited. Vascular smooth muscle cells (VSMCs) play a [...] Read more.
Background: Abdominal aortic aneurysm (AAA) is a vascular disease with a high mortality rate upon rupture (85–90%). Surgical repair remains the most effective intervention, whereas pharmacological treatments to prevent aneurysm expansion or rupture are limited. Vascular smooth muscle cells (VSMCs) play a crucial role in AAA pathogenesis, and metabolic dysregulation is increasingly recognized as a contributor to disease progression. This study investigated metabolic changes in VSMCs and their association with AAA pathology using untargeted metabolomics. Methods: Angiotensin II (Ang II) was used to stimulate rat VSMCs and induce AAA in ApoE−/− mice. Untargeted metabolomic analysis was performed using liquid chromatography–tandem mass spectrometry to detect metabolite changes. Differential metabolites were identified using orthogonal partial least squares discriminant analysis, and metabolic pathways were analyzed using Kyoto Encyclopedia of Genes and Genomes and metabolic set enrichment analysis. Results: In Ang II-treated VSMCs, 54 differential metabolites (24 upregulated; 30 downregulated) were identified, whereas 470 differential metabolites (206 upregulated; 264 downregulated) were detected in mouse aortas. Three metabolites—carnitine, lysophosphatidylcholine (0:0/20:4), and 5-hydroxyeicosatetraenoic acid—were common in both models and were enriched in bile secretion and tryptophan metabolism pathways. The carnitine–FXR signaling axis emerged as a potential therapeutic target. Conclusions: This study revealed Ang II-induced metabolic changes in VSMCs and their association with AAA pathology. The carnitine–FXR signaling axis may contribute to AAA development, providing new directions for diagnostic biomarkers and therapeutic targets. Future studies should validate these findings in human AAA samples to determine their clinical relevance. Full article
(This article belongs to the Special Issue Aortic Aneurysm: Mechanisms, Biomarkers, and Therapeutic Strategy)
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10 pages, 613 KB  
Article
Associations Between MicroRNA and Abdominal Aortic Aneurysm Diameter Differ by Sex
by Jonas Wallinder, Anne Kunath, Dick Wågsäter, Martin Björck and Anders Wanhainen
Biomedicines 2026, 14(3), 507; https://doi.org/10.3390/biomedicines14030507 - 25 Feb 2026
Viewed by 637
Abstract
Objective: Abdominal aortic aneurysm (AAA) epidemiology differs significantly between the sexes; the biological factors behind this are mostly unknown. MicroRNAs (miRNAs) are short RNA molecules providing post-transcriptional regulation of protein synthesis. Several miRNAs have been associated with the development and growth of AAA, [...] Read more.
Objective: Abdominal aortic aneurysm (AAA) epidemiology differs significantly between the sexes; the biological factors behind this are mostly unknown. MicroRNAs (miRNAs) are short RNA molecules providing post-transcriptional regulation of protein synthesis. Several miRNAs have been associated with the development and growth of AAA, but only in men. We investigated whether the associations between some selected miRNAs and aortic size differ by sex and the possible target pathways for such differences. Methods: A cross-sectional study included subjects with AAA (30–58 mm) and normal aortas. Clinical data were collected through questionnaires. Abdominal aortic diameters were measured using ultrasound. The levels of 17 miRNAs were measured in plasma. The association between miRNA levels, aortic diameter, and sex were analysed using multivariable linear regression. Results: A total of 242 subjects were included, with 85 women and 157 men. In the group with aortic diameters below 30 mm were 122 men (15–29 mm) and 50 women (13–29 mm). There were 35 men (30–54 mm) and 35 women (30–58 mm) with AAA. The associations between six miRNAs and aortic diameter were influenced by sex: miR-125 (p = 0.013), miR-128–1 (p = 0.017), miR-24 (p = 0.013), miR-26a (p = 0.022), miR-93 (p = 0.0015), and miR-194 (p = 0.013). Bioinformatic analysis indicated Hippo and TGF-beta as the two signalling pathways most likely affected by these differences. Conclusions: This exploratory study found sex differences in the associations between miRNA levels and aortic diameter, involving signalling pathways that control organ size and maintain tissue homeostasis by regulating cell proliferation, survival, and differentiation. Full article
(This article belongs to the Special Issue Aortic Aneurysm: Mechanisms, Biomarkers, and Therapeutic Strategy)
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Review

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13 pages, 961 KB  
Review
Spinal Cord Ischemia Following Thoracoabdominal Aortic Aneurysm Repair: Translational Insights from Stroke and Traumatic Injury for Biomarker Development
by James A. Kelly, Miranda Witheford, Kong Teng Tan, Tiam Feridooni, Daniyal Mahmood, Carmen Garcia-Mere and Thomas F. Lindsay
Biomedicines 2026, 14(5), 1144; https://doi.org/10.3390/biomedicines14051144 - 18 May 2026
Viewed by 623
Abstract
Background: Spinal cord ischemia (SCI) is a severe complication of thoracoabdominal aortic aneurysm (TAAA) repair, associated with substantial morbidity and mortality. Despite advances in operative techniques, its pathophysiology remains incompletely understood, with no reliable biomarkers available for early detection or risk stratification. Methods: [...] Read more.
Background: Spinal cord ischemia (SCI) is a severe complication of thoracoabdominal aortic aneurysm (TAAA) repair, associated with substantial morbidity and mortality. Despite advances in operative techniques, its pathophysiology remains incompletely understood, with no reliable biomarkers available for early detection or risk stratification. Methods: This narrative review synthesizes current evidence on the pathophysiology of SCI following aortic intervention, integrating insights from ischemic stroke and traumatic spinal cord injury to identify key mechanistic pathways and potential biomarker targets. Results: SCI results from multifactorial impairment of spinal cord perfusion pressure (SCPP) driven by extensive aortic coverage, disruption of segmental arterial inflow, hypotension, and impaired collateral circulation. While acute hypoperfusion initiates injury, secondary processes—including excitotoxicity, oxidative stress, and neuroinflammation—drive progression. Cytokine signaling and immune activation contribute to blood–spinal cord barrier disruption and vasogenic edema, with Aquaporin-4 playing a central role in delayed injury. Candidate biomarkers, including neuron-specific enolase, S100β, and glial fibrillary acidic protein, reflect neuronal damage but lack sufficient sensitivity and temporal resolution for clinical use. Emerging evidence supports a multimodal biomarker approach incorporating inflammatory, structural, and Aquaporin-4-dependent edema-related pathways. Conclusions: Spinal cord ischemia following thoracoabdominal aortic aneurysm repair is a dynamic and multifactorial process in which reduced spinal cord perfusion pressure represents a final common pathway linking diverse perioperative factors to ischemic injury. Secondary mechanisms, particularly neuroinflammation and Aquaporin-4-driven vasogenic edema, play a central role in injury propagation and represent promising targets for biomarker development. Future strategies should focus on longitudinal, multimodal biomarker approaches to improve early detection, risk stratification, and therapeutic intervention. Full article
(This article belongs to the Special Issue Aortic Aneurysm: Mechanisms, Biomarkers, and Therapeutic Strategy)
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