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Rupture of blood clots: Mechanics and pathophysiology
Fibrin is the three-dimensional mechanical scaffold of protective blood clots that stop bleeding and pathological thrombi that obstruct blood vessels. Fibrin must be mechanically tough to withstand rupture, after which life-threatening pieces (thrombotic emboli) are carried downstream by blood flow....
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Association for the Advancement of Science
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7449685/ https://www.ncbi.nlm.nih.gov/pubmed/32923647 http://dx.doi.org/10.1126/sciadv.abc0496 |
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author | Tutwiler, Valerie Singh, Jaspreet Litvinov, Rustem I. Bassani, John L. Purohit, Prashant K. Weisel, John W. |
author_facet | Tutwiler, Valerie Singh, Jaspreet Litvinov, Rustem I. Bassani, John L. Purohit, Prashant K. Weisel, John W. |
author_sort | Tutwiler, Valerie |
collection | PubMed |
description | Fibrin is the three-dimensional mechanical scaffold of protective blood clots that stop bleeding and pathological thrombi that obstruct blood vessels. Fibrin must be mechanically tough to withstand rupture, after which life-threatening pieces (thrombotic emboli) are carried downstream by blood flow. Despite multiple studies on fibrin viscoelasticity, mechanisms of fibrin rupture remain unknown. Here, we examined mechanically and structurally the strain-driven rupture of human blood plasma–derived fibrin clots where clotting was triggered with tissue factor. Toughness, i.e., resistance to rupture, quantified by the critical energy release rate (a measure of the propensity for clot embolization) of physiologically relevant fibrin gels was determined to be 7.6 ± 0.45 J/m(2). Finite element (FE) simulations using fibrin material models that account for forced protein unfolding independently supported this measured toughness and showed that breaking of fibers ahead the crack at a critical stretch is the mechanism of rupture of blood clots, including thrombotic embolization. |
format | Online Article Text |
id | pubmed-7449685 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | American Association for the Advancement of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-74496852020-09-11 Rupture of blood clots: Mechanics and pathophysiology Tutwiler, Valerie Singh, Jaspreet Litvinov, Rustem I. Bassani, John L. Purohit, Prashant K. Weisel, John W. Sci Adv Research Articles Fibrin is the three-dimensional mechanical scaffold of protective blood clots that stop bleeding and pathological thrombi that obstruct blood vessels. Fibrin must be mechanically tough to withstand rupture, after which life-threatening pieces (thrombotic emboli) are carried downstream by blood flow. Despite multiple studies on fibrin viscoelasticity, mechanisms of fibrin rupture remain unknown. Here, we examined mechanically and structurally the strain-driven rupture of human blood plasma–derived fibrin clots where clotting was triggered with tissue factor. Toughness, i.e., resistance to rupture, quantified by the critical energy release rate (a measure of the propensity for clot embolization) of physiologically relevant fibrin gels was determined to be 7.6 ± 0.45 J/m(2). Finite element (FE) simulations using fibrin material models that account for forced protein unfolding independently supported this measured toughness and showed that breaking of fibers ahead the crack at a critical stretch is the mechanism of rupture of blood clots, including thrombotic embolization. American Association for the Advancement of Science 2020-08-26 /pmc/articles/PMC7449685/ /pubmed/32923647 http://dx.doi.org/10.1126/sciadv.abc0496 Text en Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC). https://creativecommons.org/licenses/by-nc/4.0/ https://creativecommons.org/licenses/by-nc/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial license (https://creativecommons.org/licenses/by-nc/4.0/) , which permits use, distribution, and reproduction in any medium, so long as the resultant use is not for commercial advantage and provided the original work is properly cited. |
spellingShingle | Research Articles Tutwiler, Valerie Singh, Jaspreet Litvinov, Rustem I. Bassani, John L. Purohit, Prashant K. Weisel, John W. Rupture of blood clots: Mechanics and pathophysiology |
title | Rupture of blood clots: Mechanics and pathophysiology |
title_full | Rupture of blood clots: Mechanics and pathophysiology |
title_fullStr | Rupture of blood clots: Mechanics and pathophysiology |
title_full_unstemmed | Rupture of blood clots: Mechanics and pathophysiology |
title_short | Rupture of blood clots: Mechanics and pathophysiology |
title_sort | rupture of blood clots: mechanics and pathophysiology |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7449685/ https://www.ncbi.nlm.nih.gov/pubmed/32923647 http://dx.doi.org/10.1126/sciadv.abc0496 |
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