Computational modelling distinguishes diverse contributors to aneurysmal progression in the Marfan aorta.

ABSTRACT: Thoracic aortic aneurysms are characterized by a progressive loss of biomechanical functionality resulting from degenerative changes in wall composition, microstructure, and mechanical properties. Among the many causes of these lesions, Marfan syndrome is the most common heritable condition, resulting from mutations to the gene that codes the elastin-associated glycoprotein fibrillin-1. Key histopathological features of the aneurysmal Marfan aorta include extensive degradation of elastic fibres, significant remodelling of fibrillar collagens and compromised smooth muscle cell function. Computational growth and remodelling models have confirmed the importance of compromised elastic fibre integrity in aneurysmal dilatation, but we show here that this contributor alone is not sufficient to de

SUBMITTER: Li DS 

PROVIDER: S-EPMC12539648 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature