ArticleArteriosclerosis, thrombosis, and vascular biology2016
Mesenchymal Stem Cells Attenuate NADPH Oxidase-Dependent High Mobility Group Box 1 Production and Inhibit Abdominal Aortic Aneurysms.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Therapeutic efficacy of mesenchymal stem cells for abdominal aortic aneurysm: a meta-analysis of preclinical studies.Stem cell research & therapy · 2022Pooled it
- Cocktail Therapy Combining SGLT2 Inhibitor, Entresto, and Adipose-Derived Mesenchymal Stem Cells Prevents Abdominal Aortic Aneurysmal Complication Syndrome in Rodents.Acta Cardiologica Sinica · 2026Article
- Emerging Mechanisms of Abdominal Aortic Aneurysm.Current atherosclerosis reports · 2026Review
- Antisense oligonucleotide inhibition of HMGB1 attenuates angiotensin II-induced abdominal aortic aneurysms.Atherosclerosis · 2025Article
- Review
- Stem cell-based therapies for treatment of abdominal aortic aneurysm: development, application, and future potential.npj biomedical innovations · 2025Review
- Therapeutic Targeting of Signaling Pathways in Abdominal Aortic Aneurysm: From Pathogenesis to Precision Medicine.Drug design, development and therapy · 2025Review
- Immune Checkpoints Are New Therapeutic Targets in Regulating Cardio-, and Cerebro-Vascular Diseases and CD4International journal of drug discovery and pharmacology · 2024Article
- Differential Expression of Circulating Damage-Associated Molecular Patterns in Patients with Coronary Artery Ectasia.Biomolecules · 2023Article
- Novel pharmacological approaches in abdominal aortic aneurysm.Clinical science (London, England : 1979) · 2023Review
- A review of current status of cell-based therapies for aortic aneurysms.Inflammation and regeneration · 2023Review
- Treatment With Small Molecule Inhibitors of Advanced Glycation End-Products Formation and Advanced Glycation End-Products-Mediated Collagen Cross-Linking Promotes Experimental Aortic Aneurysm Progression in Diabetic Mice.Journal of the American Heart Association · 2023Article
- MicroRNA-19b-3p dysfunction of mesenchymal stem cell-derived exosomes from patients with abdominal aortic aneurysm impairs therapeutic efficacy.Journal of nanobiotechnology · 2023Article
- ER stress mediates Angiotensin II-augmented innate immunity memory and facilitates distinct susceptibilities of thoracic from abdominal aorta to aneurysm development.Frontiers in immunology · 2023Article
- Pharmacologic inhibition by spironolactone attenuates experimental abdominal aortic aneurysms.Frontiers in cardiovascular medicine · 2023Article
- Identification of Novel Plasma Biomarkers for Abdominal Aortic Aneurysm by Protein Array Analysis.Biomolecules · 2022Article
- Resolution of inflammation via RvD1/FPR2 signaling mitigates Nox2 activation and ferroptosis of macrophages in experimental abdominal aortic aneurysms.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- NADPH Oxidases in Aortic Aneurysms.Antioxidants (Basel, Switzerland) · 2022Review
- Development of pharmacotherapies for abdominal aortic aneurysms.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Endothelial pannexin-1 channels modulate macrophage and smooth muscle cell activation in abdominal aortic aneurysm formation.Nature communications · 2022Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
objectiveAbdominal aortic aneurysm (AAA) formation is characterized by inflammation, smooth muscle activation, and matrix degradation. This study tests the hypothesis that macrophage-produced high mobility group box 1 (HMGB1) production is dependent on nicotinamide adenine dinucleotide phosphate oxidase (Nox2), which leads to increase in interleukin (IL)-17 production resulting in AAA formation and that treatment with human mesenchymal stem cells (MSCs) can attenuate this process thereby inhibiting AAA formation. APPROACH AND
resultsHuman aortic tissue demonstrated a significant increase in HMGB1 expression in AAA patients when compared with controls. An elastase-perfusion model of AAA demonstrated a significant increase in HMGB1 production in C57BL/6 (wild-type [WT]) mice, which was attenuated by MSC treatment. Furthermore, anti-HMGB1 antibody treatment of WT mice attenuated AAA formation, IL-17 production, and immune cell infiltration when compared with elastase-perfused WT mice on day 14. Elastase-perfused Nox2(-/y) mice demonstrated a significant attenuation of HMGB1 and IL-17 production, cellular infiltration, matrix metalloproteinase activity, and AAA formation when compared with WT mice on day 14. In vitro studies showed that elastase-treated macrophages from WT mice, but not from Nox2(-/y) mice, produced HMGB1, which was attenuated by MSC treatment. The production of macrophage-dependent HMGB1 involved Nox2 activation and superoxide anion production, which was mitigated by MSC treatment.
conclusionsThese results demonstrate that macrophage-produced HMGB1 leads to aortic inflammation and acts as a trigger for CD4(+) T-cell-produced IL-17 during AAA formation. HMGB1 release is dependent on Nox2 activation, which can be inhibited by MSCs leading to attenuation of proinflammatory cytokines, especially IL-17, and protection against AAA formation.
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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.