ArticleMolecular therapy. Nucleic acids2017
AP-1 Oligodeoxynucleotides Reduce Aortic Elastolysis in a Murine Model of Marfan Syndrome.
Article in Molecular therapy. Nucleic acids, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Increased Disarray of Extracellular Matrix Collagen-I Fiber Network and Compromised Biomechanics in Aortae From Marfan-Syndrome Mice Assessed Through Combined Opto-Biomechatronics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Aortic asprosin overexpression does not ameliorate disease pathophysiology in a murine model of Marfan syndrome.Scientific reports · 2026Article
- The Efficacy of Antihypertensive Drugs and miR-632 Inhibition on Parietal Remodeling in a Model of Marfan Thoracic Aortic Aneurysm.Biomolecules · 2026Article
- HDAC8-selective inhibitor PCI-34051 protects against aortic dissection by attenuating ferroptosis of vascular smooth muscle cells.Life medicine · 2026Article
- AP-1-Targeting Decoy Oligonucleotides: Mechanisms and Therapeutic Potential as Modulators of Inflammatory Pathways.Journal of cellular and molecular medicine · 2026Review
- A pilot study on the effect of severe sleep fragmentation on aorta remodelling, neuroinflammation in a rat model.Scientific reports · 2025Article
- Therapeutic Opportunities of Marfan Syndrome: Current Perspectives.Drug design, development and therapy · 2025Review
- Regnase-1 overexpression as a therapeutic approach of Marfan syndrome.Molecular therapy. Methods & clinical development · 2024Article
- The role of transcription factors in the pathogenesis and therapeutic targeting of vascular diseases.Frontiers in cardiovascular medicine · 2024Review
- Translational Medicine: Towards Gene Therapy of Marfan Syndrome.Journal of clinical medicine · 2022Review
- Treatment With Methotrexate Associated With Lipid Core Nanoparticles Prevents Aortic Dilation in a Murine Model of Marfan Syndrome.Frontiers in cardiovascular medicine · 2022Article
- Harnessing the Therapeutic Potential of Decoys in Non-Atherosclerotic Cardiovascular Diseases: State of the Art.Journal of cardiovascular development and disease · 2021Review
- Downregulation of Filamin a Expression in the Aorta Is Correlated With Aortic Dissection.Frontiers in cardiovascular medicine · 2021Article
- AAV-Mediated Expression of AP-1-Neutralizing RNA Decoy Oligonucleotides Attenuates Transplant Vasculopathy in Mouse Aortic Allografts.Molecular therapy. Methods & clinical development · 2019Article
- The reimplantation valve-sparing aortic root replacement technique for patients with Marfan syndrome: A single-center experience.Scientific reports · 2019Article
Corrections and comments
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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
Marfan syndrome is characterized by high expression of matrix metalloproteinases (MMPs) in aortic smooth muscle cells (AoSMCs) associated with medial elastolysis and aortic root aneurysm. We aimed to reduce aortic elastolysis through decrease of MMP expression with decoy oligodeoxynucleotides (dODNs) neutralizing the transcription factor activating factor-1 (AP-1). AP-1 abundance in nuclear extracts as well as MMP-2 and MMP-9 expression were significantly increased in isolated mAoSMC of mgR/mgR Marfan mice compared to wild-type cells. Exposure to AP-1 neutralizing dODNs resulted in a significant reduction of basal and interleukin-1β-stimulated MMP expression and activity in mAoSMCs. Moreover, increased migration and formation of superoxide radical anions was substantially decreased in mAoSMCs by AP-1 dODN treatment. Aortic grafts from donor Marfan mice were treated with AP-1- dODN ex vivo and implanted as infrarenal aortic interposition grafts in mgR/mgR mice. Pretreatment of aortic grafts with AP-1 dODN led to reduced elastolysis, macrophage infiltration, and MMP activity. Permeability of the endothelial monolayer was increased for dODN in mgR/mgR aortae with observed loss of tight junction proteins ZO-1 and occludin, enabling dODN to reach the tunica media. Targeting AP-1 activity offers a new potential strategy to treat the vascular phenotype associated with Marfan syndrome.
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