Hemodynamics and Wall Mechanics of Vascular Graft Failure.
extracellular matrix
gene expression
heart defects, congenital
hemodynamics
signal transduction
Journal
Arteriosclerosis, thrombosis, and vascular biology
ISSN: 1524-4636
Titre abrégé: Arterioscler Thromb Vasc Biol
Pays: United States
ID NLM: 9505803
Informations de publication
Date de publication:
04 Apr 2024
04 Apr 2024
Historique:
medline:
4
4
2024
pubmed:
4
4
2024
entrez:
4
4
2024
Statut:
aheadofprint
Résumé
Blood vessels are subjected to complex biomechanical loads, primarily from pressure-driven blood flow. Abnormal loading associated with vascular grafts, arising from altered hemodynamics or wall mechanics, can cause acute and progressive vascular failure and end-organ dysfunction. Perturbations to mechanobiological stimuli experienced by vascular cells contribute to remodeling of the vascular wall via activation of mechanosensitive signaling pathways and subsequent changes in gene expression and associated turnover of cells and extracellular matrix. In this review, we outline experimental and computational tools used to quantify metrics of biomechanical loading in vascular grafts and highlight those that show potential in predicting graft failure for diverse disease contexts. We include metrics derived from both fluid and solid mechanics that drive feedback loops between mechanobiological processes and changes in the biomechanical state that govern the natural history of vascular grafts. As illustrative examples, we consider application-specific coronary artery bypass grafts, peripheral vascular grafts, and tissue-engineered vascular grafts for congenital heart surgery as each of these involves unique circulatory environments, loading magnitudes, and graft materials.
Identifiants
pubmed: 38572650
doi: 10.1161/ATVBAHA.123.318239
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM