| Literature DB >> 27743312 |
Mark J Osborn1,2,3,4,5, Beau R Webber6, Ronald T McElmurry6, Kyle D Rudser7, Anthony P DeFeo6, Michael Muradian6, Anna Petryk6, Benedikt Hallgrimsson7, Bruce R Blazar6, Jakub Tolar6,8,9,10, Elizabeth A Braunlin11,12.
Abstract
Mucopolysaccharidosis type I (MPS IH) is a lysosomal storage disease (LSD) caused by inactivating mutations to the alpha-L-iduronidase (IDUA) gene. Treatment focuses on IDUA enzyme replacement and currently employed methods can be non-uniform in their efficacy particularly for the cardiac and craniofacial pathology. Therefore, we undertook efforts to better define the pathological cascade accounting for treatment refractory manifestations and demonstrate a role for the renin angiotensin system (RAS) using the IDUA-/- mouse model. Perturbation of the RAS in the aorta was more profound in male animals suggesting a causative role in the observed gender dimorphism and angiotensin receptor blockade (ARB) resulted in improved cardiac function. Further, we show the ability of losartan to prevent shortening of the snout, a common craniofacial anomaly in IDUA-/- mice. These data show a key role for the RAS in MPS associated pathology and support the inclusion of losartan as an augmentation to current therapies.Entities:
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Year: 2016 PMID: 27743312 PMCID: PMC5335863 DOI: 10.1007/s10545-016-9988-z
Source DB: PubMed Journal: J Inherit Metab Dis ISSN: 0141-8955 Impact factor: 4.982