Mechanics-driven mechanobiological mechanisms of arterial tortuosity

[EN] Arterial tortuosity manifests in many conditions, including hypertension, genetic mutations predisposing to thoracic aortopathy, and vascular aging. Despite evidence that tortuosity disrupts efficient blood flow and that it may be an important clinical biomarker, underlying mechanisms remain po...

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Detalles Bibliográficos
Autores: Weiss, Dar, Cavinato, Cristina, Gray, Authia, Ramachandra, Abhay B., Avril, Stephane, Humphrey, Jay D., Latorre, Marcos|||0000-0003-4142-0207
Tipo de recurso: artículo
Fecha de publicación:2020
País:España
Institución:Universitat Politècnica de València (UPV)
Repositorio:RiuNet. Repositorio Institucional de la Universitat Politécnica de Valéncia
Idioma:inglés
OAI Identifier:oai:riunet.upv.es:10251/191511
Acceso en línea:https://riunet.upv.es/handle/10251/191511
Access Level:acceso abierto
Palabra clave:Tortuosity
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Descripción
Sumario:[EN] Arterial tortuosity manifests in many conditions, including hypertension, genetic mutations predisposing to thoracic aortopathy, and vascular aging. Despite evidence that tortuosity disrupts efficient blood flow and that it may be an important clinical biomarker, underlying mechanisms remain poorly understood but are widely appreciated to be largely biomechanical. Many previous studies suggested that tortuosity may arise via an elastic structural buckling instability, but the novel experimental-computational approach used here suggests that tortuosity arises from mechanosensitive, cell-mediated responses to local aberrations in the microstructural integrity of the arterial wall. In particular, computations informed by multimodality imaging show that aberrations in elastic fiber integrity, collagen alignment, and collagen turnover can lead to a progressive loss of structural stability that entrenches during the development of tortuosity. Interpreted in this way, microstructural defects or irregularities of the arterial wall initiate the condition and hypertension is a confounding factor.