ArticleAnnals of biomedical engineering2016
Losartan Attenuates Degradation of Aorta and Lung Tissue Micromechanics in a Mouse Model of Severe Marfan Syndrome.
Article in Annals of biomedical engineering, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 32 citations in OpenAlex.
- Neuro-Mechanical Regulation of Vascular Smooth Muscle Cell Behaviour Under Ageing-Associated Substrate Stiffness.Current issues in molecular biology · 2026Article
- Hypertension drives thoracic aortic aneurysm and dissection in male, but not female, Marfan mice.Journal of the mechanical behavior of biomedical materials · 2026Article
- Rab26 promotes hypoxia-induced hyperproliferation of PASMCs by modulating the AT1R-STAT3-YAP axis.Cellular and molecular life sciences : CMLS · 2025Article
- Cell type-specific expression of angiotensin receptors in the human lung with implications for health, aging, and chronic disease.bioRxiv : the preprint server for biology · 2024Article
- IL11 (Interleukin-11) Causes Emphysematous Lung Disease in a Mouse Model of Marfan Syndrome.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Fibrillin-1 Regulates Arteriole Integrity in the Retina.Biomolecules · 2022Article
- Elevated TGFβ signaling contributes to ocular anterior segment dysgenesis in Col4a1 mutant mice.Matrix biology : journal of the International Society for Matrix Biology · 2022Article
- Pressure and stiffness sensing together regulate vascular smooth muscle cell phenotype switching.Science advances · 2022Article
- Respiratory manifestations of Marfan syndrome: a narrative review.Journal of thoracic disease · 2021Review
- Review
- An Overview of Investigational and Experimental Drug Treatment Strategies for Marfan Syndrome.Journal of experimental pharmacology · 2021Review
- The correlation between spinal and chest wall deformities and pulmonary function in Marfan syndrome.Journal of children's orthopaedics · 2020Article
- Glycoproteomic Analysis of the Aortic Extracellular Matrix in Marfan Patients.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Sildenafil Prevents Marfan-Associated Emphysema and Early Pulmonary Artery Dilation in Mice.The American journal of pathology · 2019Article
- The Genetics of Pneumothorax.American journal of respiratory and critical care medicine · 2019Review
- Aortic Strain Correlates with Elastin Fragmentation in Fibrillin-1 Hypomorphic Mice.Circulation reports · 2019Article
- Inflammation in thoracic aortic aneurysms.Herz · 2019Article
- Marfan syndrome; A connective tissue disease at the crossroads of mechanotransduction, TGFβ signaling and cell stemness.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- Dehomogenized Elastic Properties of Heterogeneous Layered Materials in AFM Indentation Experiments.Biophysical journal · 2018Article
- Bio-chemo-mechanics of thoracic aortic aneurysms.Current opinion in biomedical engineering · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Marfan syndrome (MFS) is an autosomal dominant disease of the connective tissue due to mutations in the fibrillin-1 gene (FBN1). This study aimed at characterizing microelastic properties of the ascending aortic wall and lung parenchyma tissues from wild type (WT) and age-matched Fbn1 hypomorphic mice (Fbn1(mgR/mgR) mice) to identify tissue-specific biomechanical effects of aging and disease in MFS. Atomic force microscopy was used to indent lung parenchyma and aortic wall tissues, using Hybrid Eshelby Decomposition analysis to extract layer-specific properties of the intima and media. The intima stiffened with age and was not different between WT and Fbn1(mgR/mgR) tissues, whereas the media layer of MFS aortas showed progressive structural and mechanical degradation with a modulus that was 50% softer than WT by 3.5 months of age. Similarly, MFS mice displayed progressive structural and mechanical deterioration of lung tissue, which was over 85% softer than WT by 3.5 months of age. Chronic treatment with the angiotensin type I receptor antagonist, losartan, attenuated the aorta and lung tissue degradation, resulting in structural and mechanical properties not significantly different from age-matched WT controls. By revealing micromechanical softening of elastin-rich aorta and lung tissues with disease progression in fibrillin-1 deficient mice, our findings support the use of losartan as a prophylactic treatment that may abrogate the life-threatening symptoms of MFS.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.