ArticleNature communications2021
Aortic disease in Marfan syndrome is caused by overactivation of sGC-PRKG signaling by NO.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 55 citations in OpenAlex.
- The aorta in Marfan syndrome: from molecular mechanisms to mechanobiological dysfunction.Cardiovascular research · 2026Review
- Chiral Nanoparticles Suppress Inflammatory Infiltration to Promote Extracellular Matrix Remodeling for Ectopia Lentis Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Heritable Thoracic Aortic Diseases in Pediatric Practice: From Molecular Mechanisms to Genotype-Informed Management, a Comprehensive Narrative Review.Journal of clinical medicine · 2026Review
- Fibronectin-induced overactivation of αNature communications · 2026Article
- Mechanotransduction in Marfan Syndrome and Related Aortic Disorders: Insights from Transcriptomic Analyses.Genes · 2026Review
- A multiscale computational model of ascending thoracic aortic aneurysm development in Marfan syndrome for in silico trials.Biomechanics and modeling in mechanobiology · 2026Article
- Ultrasound-guided left heart injection: a safer and more efficient strategy for mouse thoracic aortic gene delivery.Gene therapy · 2026Article
- Aortic dissection: the role of macrophages in disease pathogenesis and their potential as a treatment target.Journal of cardiothoracic surgery · 2026Review
- Mitochondrial dysfunction in aortic aneurysm and dissection: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Calcium channel blockers increase the risk of aortic aneurysm and dissection.Nature communications · 2025Article
- Vascular Smooth Muscle Cell Metabolic Disorders in the Occurrence and Development of Aortic Aneurysms and Dissections: Implications for Therapy.Biomedicines · 2025Review
- VASP Knockdown Ameliorates Lipopolysaccharide-Induced Acute Lung Injury with Inhibition of M1 Macrophage Polarization Through the cGMP-PKG Signaling Pathway.Inflammation · 2025Article
- Smooth Muscle Cell-Derived Fibronectin Promotes an Atheroprotective Smooth Muscle Cell Phenotype Associated With Altered NO-cGMP Signaling.Journal of the American Heart Association · 2025Article
- Nitric Oxide Distribution Correlates with Intraluminal Thrombus in Abdominal Aortic Aneurysm: A Computational Study.Bioengineering (Basel, Switzerland) · 2025Article
- Inhibition of aortic CX3CR1+ macrophages mitigates thoracic aortic aneurysm progression in Marfan syndrome in mice.The Journal of clinical investigation · 2025Article
- Fibrillin-1 Deficiency Perturbs Aortic Cholinergic Relaxation and Adrenergic Contraction in a Mouse Model of Early Onset Progressively Severe Marfan Syndrome.Journal of vascular research · 2025Article
- iSanXoT: A standalone application for the integrative analysis of mass spectrometry-based quantitative proteomics data.Computational and structural biotechnology journal · 2024Article
- A Multiplexed Quantitative Proteomics Approach to the Human Plasma Protein Signature.Biomedicines · 2024Article
- The perspective of cAMP/cGMP signaling and cyclic nucleotide phosphodiesterases in aortic aneurysm and dissection.Vascular pharmacology · 2024Review
- Animal Models, Pathogenesis, and Potential Treatment of Thoracic Aortic Aneurysm.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
21 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thoracic aortic aneurysm, as occurs in Marfan syndrome, is generally asymptomatic until dissection or rupture, requiring surgical intervention as the only available treatment. Here, we show that nitric oxide (NO) signaling dysregulates actin cytoskeleton dynamics in Marfan Syndrome smooth muscle cells and that NO-donors induce Marfan-like aortopathy in wild-type mice, indicating that a marked increase in NO suffices to induce aortopathy. Levels of nitrated proteins are higher in plasma from Marfan patients and mice and in aortic tissue from Marfan mice than in control samples, indicating elevated circulating and tissue NO. Soluble guanylate cyclase and cGMP-dependent protein kinase are both activated in Marfan patients and mice and in wild-type mice treated with NO-donors, as shown by increased plasma cGMP and pVASP-S239 staining in aortic tissue. Marfan aortopathy in mice is reverted by pharmacological inhibition of soluble guanylate cyclase and cGMP-dependent protein kinase and lentiviral-mediated Prkg1 silencing. These findings identify potential biomarkers for monitoring Marfan Syndrome in patients and urge evaluation of cGMP-dependent protein kinase and soluble guanylate cyclase as therapeutic targets.
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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.