Losartan, an AT1 Antagonist, Prevents Aortic Aneurysm in a Mouse Model of Marfan Syndrome

By J. Habashi, D. Judge, Tammy M. Holm, R. Cohn, B. Loeys, T. Cooper, Loretha A Myers, E. C. Klein, Guosheng Liu, C. Calvi and 10 more. Science, 2006

1,772 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/5e58aba28865d71710e0b44249788b63ea132cfa

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In Genetics

In Molecular Biology

In Pulmonary and Respiratory Medicine

Rakesh K. Jain

Citations in the corpus

Losartan inhibits collagen I synthesis and improves the distribution and efficacy of nanotherapeutics in tumors (2011, background): “Furthermore, in addition to its antihypertensive properties, losartan is also an antifibrotic agent that has been shown to reduce the incidence of cardiac and renal fibrosis (15, 16).”
ADAMTS proteins as modulators of microfibril formation and function (2015, background): “In mice recapitulating a MFS-causing FBN1 mutation, dysregulation (excess) of TGFβ signaling contributed to the pathology of aortic aneurysm and pulmonary emphysema [52,53].”
High-throughput screening assays for the identification of chemical probes. (2007, background): “Occasionally a rare disease is caused by mutation of an immediately druggable target, and even more rarely one that may be ameliorated by a clinically approved dru”
The revised Ghent nosology for the Marfan syndrome (2010, background): “β-blockade should be considered in all patients with MFS, including children and those with aortic root diameters”
Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease (2010, background): “Recent studies in a mouse model of Marfan syndrome with aortic disease similar to that seen in humans showed that treatment with losartan normalized aortic root growth (6), and a clinical trial using losartan in Marfan syndrome patients under the age of 25 years is in progress (89,90) (see Section 9”
Wound repair and regeneration: Mechanisms, signaling, and translation (2014, neutral): “Thus, although caused by a mutation in an ECM molecule, selected disease manifestations of Marfan syndrome reflect disturbances in TGF β signaling (138).”
Angiotensin II type 1 receptor blockade attenuates TGF-β–induced failure of muscle regeneration in multiple myopathic states (2007, background): “Analyses of fibrillin-1–deficient mice showed that enhanced activation of and signaling by TGF-β contributes directly to failed distal alveolar septation, myxomatous changes of the atrioventricular valves and aortic aneurysm formatio”