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Biomolecules
Special Issues
Molecular and Cellular Mechanisms of Aortic Diseases
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Molecular and Cellular Mechanisms of Aortic Diseases

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (28 February 2026) | Viewed by 4775

Special Issue Editor

Dr. Maria Giovanna Scioli

E-Mail Website
Guest Editor
Department of Biomedicine and Prevention, Tor Vergata University of Rome, 00133 Rome, Italy
Interests: oxidative stress; platelet-rich plasmas; stem cells; medicines; biology; hair re-growth in androgenetic alopecia
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

I am pleased to invite you to submit original research articles and reviews on the topic of molecular and cellular mechanisms of aortic diseases. Aortic diseases are a group of acute and chronic conditions, whose severity varies significantly from emergency and life-threatening to conservatively managed conditions. Among those pathologies, we include aortic aneurysms and acute aortic syndromes, including aortic dissection, intramural haematoma, penetrating atherosclerotic ulcer and traumatic aortic injury, pseudoaneurysm, aortic rupture, and atherosclerotic and inflammatory affections, as well as genetic diseases (e.g., Marfan syndrome) and congenital abnormalities including the coarctation of the aorta. Papers focused on the molecular/cellular changes underlying the pathogenetic mechanisms of aortic diseases (both thoracic and abdominal) and their progression are welcomed. The aim of this Special Issue is to deepen our understanding of these pathologies in order to identify new diagnostic and prognostic markers, as well as innovative targeted therapies for more personalized therapeutic approaches.

I look forward to receiving your contributions.

Dr. Maria Giovanna Scioli
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules 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 2700 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
  • acute aortic syndromes
  • aortic dissection
  • intramural haematoma
  • penetrating atherosclerotic ulcer
  • traumatic aortic injury
  • pseudoaneurysm
  • aortic rupture
  • atherosclerotic
  • inflammatory affections
  • Marfan syndrome
  • congenital abnormalities
  • aortic diseases

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Published Papers (4 papers)

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Research

Jump to: Review

24 pages, 3063 KB  
Article
Thoracic Aortic Aneurysm Development Is Dependent on Membrane Type-1 Matrix Metalloproteinase Activity and Abundance
by Ying Xiong, Rupak Mukherjee, Sarah L. Lieser, Adam W. Akerman, Robert E. Stroud, Elizabeth K. Nadeau, Francis G. Spinale, John S. Ikonomidis and Jeffrey A. Jones
Biomolecules 2026, 16(2), 237; https://doi.org/10.3390/biom16020237 - 3 Feb 2026
Viewed by 628
Abstract
Thoracic aortic aneurysm (TAA) results from dysregulated remodeling of the extracellular matrix mediated by matrix metalloproteinase (MMP) activity. Previous studies identified elevated membrane type-1 MMP (MT1-MMP) abundance and activity during TAA development and suggested aortic fibroblasts as a potential key source. Herein, we [...] Read more.
Thoracic aortic aneurysm (TAA) results from dysregulated remodeling of the extracellular matrix mediated by matrix metalloproteinase (MMP) activity. Previous studies identified elevated membrane type-1 MMP (MT1-MMP) abundance and activity during TAA development and suggested aortic fibroblasts as a potential key source. Herein, we extended our understanding of the role of MT1-MMP during TAA development using various MT1-MMP transgenic mouse strains. MT1-MMP deficient (MT1-MMP+/−) mice exhibited reduced MT1-MMP abundance, activity, and collagen volume fraction following TAA induction, concomitant with reduced aortic dilatation. TAA tissue from wild-type and MT1-MMP+/− mice showed a similar reduction in thin collagen fibers, while the MT1-MMP+/− mice displayed no change in thick collagen fibers. The role of fibroblast-derived MT1-MMP was examined using a conditional fibroblast-specific tamoxifen-inducible MT1-MMP knockout strain (FbMT1KO). TAA-induced changes in aortic diameter and MT1-MMP abundance were attenuated in FbMT1KO mice. Using aortic fibroblasts isolated from multiple mouse strains expressing different levels of MT1-MMP, a significant correlation between MT1-MMP abundance and TGF-β activation was observed. Importantly, treatment with MT1-MMP activity-neutralizing antibody or TGF-β neutralizing antibody resulted in the attenuation aortic dilatation. Together, these findings suggest that fibroblast-derived MT1-MMP is required for TAA development, in part through its ability to induce TGF-β signaling. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Aortic Diseases)
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16 pages, 10359 KB  
Article
Gamma-Oryzanol Attenuates Aortic Valve Interstitial Cell Calcification via Suppression of BMP2-SMAD and MAPK Signaling Pathways
by Mausam Thapa, Saugat Shiwakoti, Dalseong Gong, Ju-Young Ko, Yeon-Hyang Gwak and Min-Ho Oak
Biomolecules 2026, 16(1), 107; https://doi.org/10.3390/biom16010107 - 8 Jan 2026
Viewed by 800
Abstract
Calcific aortic valve stenosis (CAVS) is a progressive cardiovascular disease associated with oxidative stress-driven osteogenic differentiation of valvular interstitial cells (VICs), yet no pharmacological therapy can prevent its progression. γ-oryzanol (γ-ORZ), a rice bran-derived phytosteryl ferulate, exhibits potent antioxidative and anti-inflammatory activities that [...] Read more.
Calcific aortic valve stenosis (CAVS) is a progressive cardiovascular disease associated with oxidative stress-driven osteogenic differentiation of valvular interstitial cells (VICs), yet no pharmacological therapy can prevent its progression. γ-oryzanol (γ-ORZ), a rice bran-derived phytosteryl ferulate, exhibits potent antioxidative and anti-inflammatory activities that may counteract valvular calcification. Here, we show that γ-ORZ markedly attenuates PCM-induced intracellular ROS elevation, osteogenic differentiation, and calcium phosphate deposition in porcine VICs (pVICs). In addition, RT-qPCR and Western blot analyses revealed significant downregulation of calcification markers (RUNX2, OPN, BMP2), along with suppressed SMAD1/5/9 transcription and phosphorylation, decreased p38/ERK MAPK activation, and reduced ALP activity. Collectively, these findings indicate that γ-ORZ mitigates oxidative stress-mediated valvular calcification by inhibiting both canonical and non-canonical BMP2-SMAD/MAPK signaling, suggesting its potential as a medicinal candidate for early intervention in CAVS. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Aortic Diseases)
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Review

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21 pages, 3225 KB  
Review
Embryological Divergence and Molecular Mechanisms in Thoracic and Abdominal Aortic Aneurysms: Bridging Developmental Biology and Clinical Insights
by Mathias Van Hemelrijck, Petar Risteski, Laura Rings, Milan Milojevic, Héctor Rodríguez Cetina Biefer and Omer Dzemali
Biomolecules 2025, 15(12), 1654; https://doi.org/10.3390/biom15121654 - 26 Nov 2025
Viewed by 989
Abstract
Aortic aneurysms are complex, predominantly asymptomatic vascular diseases with distinct incidence patterns depending on anatomical localisation. The incidence of thoracic aortic aneurysms (TAAs) has moderately increased, whereas that of abdominal aortic aneurysms has declined, primarily due to public health measures. Undiagnosed or poorly [...] Read more.
Aortic aneurysms are complex, predominantly asymptomatic vascular diseases with distinct incidence patterns depending on anatomical localisation. The incidence of thoracic aortic aneurysms (TAAs) has moderately increased, whereas that of abdominal aortic aneurysms has declined, primarily due to public health measures. Undiagnosed or poorly managed aneurysms are at significant risk of progression to acute aortic syndrome, with high associated mortality. The embryological origins of the aorta may have a substantial impact on its structural, cellular, and functional heterogeneity. Specifically, smooth-muscle cells (SMCs) in the thoracic aorta are derived from cardiac neural crest and mesodermal cells, whereas abdominal aortic SMCs originate from the paraxial and splanchnic mesoderm. To explore these developmental and regional distinctions, we conducted a narrative review based on targeted literature retrieval and expert curation, highlighting how these distinctions might potentially influence susceptibility to aneurysms and their clinical presentation. Histological differences, such as the number of lamellar units and the presence or absence of vasa vasorum, could further explain regional vulnerability. Molecular mechanisms underlying aneurysm formation include inflammation, oxidative stress, extracellular matrix degradation, phenotypic switching, and dysregulated signalling pathways, notably transforming growth factor-beta (TGF-β) and angiotensin II. Genetic mutations significantly contribute to TAAs, with genes involved in the elastin–contractile unit and TGF-β signalling pathways playing pivotal roles. However, the complex interplay between genetic susceptibility and risk factors explains why some patients develop aneurysms while others do not. Clinical management strategies have evolved, emphasising early risk stratification, surveillance, and timely surgical intervention, guided increasingly by genetic profiling and segment-specific molecular understanding. Advances in genomic technologies, biomarker identification, and computational modelling promise to enhance individualised care. Bridging developmental biology, molecular genetics, and clinical practice is crucial for improving outcomes in patients with aortic aneurysms, thereby reinforcing a multidisciplinary approach to patient-centred cardiovascular medicine. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Aortic Diseases)
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19 pages, 1123 KB  
Review
Extracellular Vesicles in Calcific Aortic Valve Disease: From Biomarkers to Drug Delivery Applications
by Alberto Cook-Calvete, Maria Delgado-Marin, Blanca Fernandez-Rodriguez, Carlos Zaragoza and Marta Saura
Biomolecules 2025, 15(11), 1548; https://doi.org/10.3390/biom15111548 - 4 Nov 2025
Cited by 1 | Viewed by 2015
Abstract
Calcific aortic valve disease (CAVD) is a progressive disorder where molecular alterations occur long before visible calcification, making early biomarkers essential. Extracellular vesicles (EVs) have gained attention as stable biomarkers due to their lipid bilayer, which protects proteins, lipids, and RNAs, ensuring reliable [...] Read more.
Calcific aortic valve disease (CAVD) is a progressive disorder where molecular alterations occur long before visible calcification, making early biomarkers essential. Extracellular vesicles (EVs) have gained attention as stable biomarkers due to their lipid bilayer, which protects proteins, lipids, and RNAs, ensuring reliable detection even in archived samples. This review highlights the role of EVs as biomarkers and delivery tools in CAVD. EVs derived from valvular endothelial, interstitial, and immune cells carry disease-specific signatures, including osteogenic proteins (BMP-2, Annexins), inflammatory miRNAs (miR-30b, miR-122-5p), and lipid mediators. These reflect early pathogenic processes before macroscopic calcification develops. Their presence in minimally invasive samples such as blood, urine, or saliva facilitates diagnosis, while their stability supports long-term monitoring of disease progression and therapeutic response. Advances in purification and single-EV analysis increase specificity, though challenges remain in standardizing methods and distinguishing CAVD-derived EVs from those in atherosclerosis. Beyond diagnostics, engineered EVs show promise as therapeutic carriers. Delivery of anti-calcific miRNAs or combined RNA cargos has reduced calcification and inflammation in preclinical models. Overall, EVs act as molecular mirrors of CAVD, enabling early diagnosis, risk stratification, and novel therapeutic strategies. Yet, clinical translation requires technical refinement and validation of the disease-specific signatures. Full article
(This article belongs to the Special Issue Molecular and Cellular Mechanisms of Aortic Diseases)
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