ArticleBioactive materials2024
Transcriptome analysis reveals therapeutic potential of NAMPT in protecting against abdominal aortic aneurysm in human and mouse.
Article in Bioactive materials, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 15 citations in OpenAlex.
- Hub genes of neutrophil extracellular traps in abdominal aortic aneurysm: a bioinformatics analysis.Hereditas · 2026Article
- Metabolic reprogramming in aortic diseases: insights from metabolomics and therapeutic opportunities.Medical review (2021) · 2026Review
- Emerging Mechanisms of Abdominal Aortic Aneurysm.Current atherosclerosis reports · 2026Review
- Role of Extracellular Vesicles in Abdominal Aortic Aneurysm: Pathophysiology, Biomarkers, and Therapeutic Potentials.International journal of molecular sciences · 2026Review
- Piezo1 Impairs Endothelial Barrier and Drives Aortic Aneurysm and Dissection via STAT3-Dependent Activation of the CCL2-CCR2 Axis.Research (Washington, D.C.) · 2026Article
- Transcriptomic Association of COL3A1Pain research & management · 2026Article
- Dissection of Microglial Heterogeneity and Identification of Pain-Related Subpopulations After Traumatic Brain Injury.Pain research & management · 2026Article
- Extracellular vesicles for abdominal aortic aneurysm: mechanisms, therapeutic potential, and translational challenges.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Single-cell landscape of melanoma reveals ETV5-driven C3 ID4Frontiers in immunology · 2026Article
- Extracellular Vesicles in Calcific Aortic Valve Disease: From Biomarkers to Drug Delivery Applications.Biomolecules · 2025Review
- Engineering biomimetic nanovesicles for PEBP1 mRNA delivery to inhibit ferroptosis in abdominal aortic aneurysm.Bioengineering & translational medicine · 2025Article
- Annexin-A1 deficiency uncovers female-specific pathways in blood pressure control and cardiovascular remodeling in mice.Communications biology · 2025Article
- The Pathophysiological Role of Vascular Smooth Muscle Cells in Abdominal Aortic Aneurysm.Cells · 2025Review
- Secretome enriched with small extracellular vesicles derived from human gingiva-derived mesenchymal stem cells enhances rat tongue muscle regeneration.Journal of nanobiotechnology · 2025Article
- Macrophage-derived KIF13B interacts with USP9X to attenuate abdominal aortic aneurysm development by potentiating TFEB stability.Theranostics · 2025Article
- Ciprofloxacin Accelerates Angiotensin-II-Induced Vascular Smooth Muscle Cells Senescence Through Modulating AMPK/ROS pathway in Aortic Aneurysm and Dissection.Cardiovascular toxicology · 2024Article
- The role of nicotinamide adenine dinucleotide salvage enzymes in cardioprotection.Kardiochirurgia i torakochirurgia polska = Polish journal of cardio-thoracic surgery · 2024Review
- LncRNA CARMN inhibits abdominal aortic aneurysm formation and vascular smooth muscle cell phenotypic transformation by interacting with SRF.Cellular and molecular life sciences : CMLS · 2024Article
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abdominal Aortic Aneurysm (AAA) is a life-threatening vascular disease characterized by the weakening and ballooning of the abdominal aorta, which has no effective therapeutic approaches due to unclear molecular mechanisms. Using single-cell RNA sequencing, we analyzed the molecular profile of individual cells within control and AAA abdominal aortas. We found cellular heterogeneity, with increased plasmacytoid dendritic cells and reduced endothelial cells and vascular smooth muscle cells (VSMCs) in AAA. Up-regulated genes in AAA were associated with muscle tissue development and apoptosis. Genes controlling VSMCs aberrant switch from contractile to synthetic phenotype were significantly enriched in AAA. Additionally, VSMCs in AAA exhibited cell senescence and impaired oxidative phosphorylation. Similar observations were made in a mouse model of AAA induced by Angiotensin II, further affirming the relevance of our findings to human AAA. The concurrence of gene expression changes between human and mouse highlighted the impairment of oxidative phosphorylation as a potential target for intervention. Nicotinamide phosphoribosyltransferase (NAMPT, also named VISFATIN) signaling emerged as a signature event in AAA. NAMPT was significantly downregulated in AAA. NAMPT-extracellular vesicles (EVs) derived from mesenchymal stem cells restored NAMPT levels, and offered protection against AAA. Furthermore, NAMPT-EVs not only repressed injuries, such as cell senescence and DNA damage, but also rescued impairments of oxidative phosphorylation in both mouse and human AAA models, suggesting NAMPT supplementation as a potential therapeutic approach for AAA treatment. These findings shed light on the cellular heterogeneity and injuries in AAA, and offered promising therapeutic intervention for AAA treatment.
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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 OpenQuestion graph.