ReviewCells2024
Cellular, Molecular and Clinical Aspects of Aortic Aneurysm-Vascular Physiology and Pathophysiology.
Review in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- Structural and transcriptomic alterations underlying the progression of aortic dissection in Fbn1Scientific reports · 2026Article
- Burden of aortic aneurysm and lead exposure risk factor in adults aged 60 years and older from 1990 to 2021: a global, regional, and national analysis.Frontiers in public health · 2026Article
- Embryological Divergence and Molecular Mechanisms in Thoracic and Abdominal Aortic Aneurysms: Bridging Developmental Biology and Clinical Insights.Biomolecules · 2025Review
- Obesity: An Underlying Risk for Acute Aortic Dissection.Journal of clinical medicine · 2025Review
- The Involvement of Herpesviruses in the Pathogenesis of Thoracic Aortic Aneurysms: Passive Bystanders or Active Contributors?Reviews in cardiovascular medicine · 2025Review
- The role of m6A methylation in abdominal aortic aneurysms: Mechanisms, progress and future perspectives (Review).Molecular medicine reports · 2025Review
- Extracellular matrix in vascular homeostasis and disease.Nature reviews. Cardiology · 2025Review
- Article
- Molecular Insights into Cardiovascular Disease: Unraveling Pathways for Diagnosis and Treatment.International journal of molecular sciences · 2025Article
- Genetic factors and management strategies in aortic health: a literature review of inherited aortopathy.Annals of medicine and surgery (2012) · 2025Review
- Therapeutic Targeting of Signaling Pathways in Abdominal Aortic Aneurysm: From Pathogenesis to Precision Medicine.Drug design, development and therapy · 2025Review
- Neutrophil extracellular traps: emerging drivers and therapeutic targets in abdominal aortic aneurysm pathogenesis.Experimental biology and medicine (Maywood, N.J.) · 2025Review
- Vascular Mesenchymal Stromal Cells and Cellular Senescence: A Two-Case Study Investigating the Correlation Between an Inflammatory Microenvironment and Abdominal Aortic Aneurysm Development.International journal of molecular sciences · 2024Article
- Article
- Elucidating VSMC phenotypic transition mechanisms to bridge insights into cardiovascular disease implications.Frontiers in cardiovascular medicine · 2024Review
- Microarray Analysis of Human Abdominal Aortic Aneurysm With Emphasis on Cardiovascular Genes Revealed Differentially Expressed Genes.In vivo (Athens, Greece)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 4 countries.
Funding
Abstract
A disturbance of the structure of the aortic wall results in the formation of aortic aneurysm, which is characterized by a significant bulge on the vessel surface that may have consequences, such as distention and finally rupture. Abdominal aortic aneurysm (AAA) is a major pathological condition because it affects approximately 8% of elderly men and 1.5% of elderly women. The pathogenesis of AAA involves multiple interlocking mechanisms, including inflammation, immune cell activation, protein degradation and cellular malalignments. The expression of inflammatory factors, such as cytokines and chemokines, induce the infiltration of inflammatory cells into the wall of the aorta, including macrophages, natural killer cells (NK cells) and T and B lymphocytes. Protein degradation occurs with a high expression not only of matrix metalloproteinases (MMPs) but also of neutrophil gelatinase-associated lipocalin (NGAL), interferon gamma (IFN-γ) and chymases. The loss of extracellular matrix (ECM) due to cell apoptosis and phenotype switching reduces tissue density and may contribute to AAA. It is important to consider the key mechanisms of initiating and promoting AAA to achieve better preventative and therapeutic outcomes.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.