Details
| Original language | English |
|---|---|
| Pages (from-to) | 539-552 |
| Number of pages | 14 |
| Journal | Biomechanics and Modeling in Mechanobiology |
| Volume | 23 |
| Issue number | 2 |
| Early online date | 23 Dec 2023 |
| Publication status | Published - Apr 2024 |
Abstract
Atherosclerosis is a disease in blood vessels that often results in plaque formation and lumen narrowing. It is an inflammatory response of the tissue caused by disruptions in the vessel wall nourishment. Blood vessels are nourished by nutrients originating from the blood of the lumen. In medium-sized and larger vessels, nutrients are additionally provided from outside through a network of capillaries called vasa vasorum. It has recently been hypothesized (Haverich in Circulation 135:205–207, 2017) that the root of atherosclerotic diseases is the malfunction of the vasa vasorum. This, so-called outside-in theory, is supported by a recently developed numerical model (Soleimani et al. in Arch Comput Methods Eng 28:4263–4282, 2021) accounting for the inflammation initiation in the adventitial layer of the blood vessel. Building on the previous findings, this work proposes an extended material model for atherosclerosis formation that is based on the outside-in theory. Beside the description of growth kinematics and nutrient diffusion, the roles of monocytes, macrophages, foam cells, smooth muscle cells and collagen are accounted for in a nonlinear continuum mechanics framework. Cells are activated due to a lack of vessel wall nourishment and proliferate, migrate, differentiate and synthesize collagen, leading to the formation of a plaque. Numerical studies show that the onset of atherosclerosis can qualitatively be reproduced and back the new theory.
Keywords
- Atherosclerosis, Finite element method, Mechanobiology, Outside-in theory
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Biotechnology
- Mathematics(all)
- Modelling and Simulation
- Engineering(all)
- Mechanical Engineering
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In: Biomechanics and Modeling in Mechanobiology, Vol. 23, No. 2, 04.2024, p. 539-552.
Research output: Contribution to journal › Article › Research › peer review
}
TY - JOUR
T1 - Mechano-chemo-biological model of atherosclerosis formation based on the outside-in theory
AU - Gierig, Meike
AU - Tragoudas, Alexandros
AU - Haverich, Axel
AU - Wriggers, Peter
N1 - Funding Information: P. Wriggers gratefully acknowledges the support by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) - SFB/TRR-298-SIIRI - Project-ID 426335750.
PY - 2024/4
Y1 - 2024/4
N2 - Atherosclerosis is a disease in blood vessels that often results in plaque formation and lumen narrowing. It is an inflammatory response of the tissue caused by disruptions in the vessel wall nourishment. Blood vessels are nourished by nutrients originating from the blood of the lumen. In medium-sized and larger vessels, nutrients are additionally provided from outside through a network of capillaries called vasa vasorum. It has recently been hypothesized (Haverich in Circulation 135:205–207, 2017) that the root of atherosclerotic diseases is the malfunction of the vasa vasorum. This, so-called outside-in theory, is supported by a recently developed numerical model (Soleimani et al. in Arch Comput Methods Eng 28:4263–4282, 2021) accounting for the inflammation initiation in the adventitial layer of the blood vessel. Building on the previous findings, this work proposes an extended material model for atherosclerosis formation that is based on the outside-in theory. Beside the description of growth kinematics and nutrient diffusion, the roles of monocytes, macrophages, foam cells, smooth muscle cells and collagen are accounted for in a nonlinear continuum mechanics framework. Cells are activated due to a lack of vessel wall nourishment and proliferate, migrate, differentiate and synthesize collagen, leading to the formation of a plaque. Numerical studies show that the onset of atherosclerosis can qualitatively be reproduced and back the new theory.
AB - Atherosclerosis is a disease in blood vessels that often results in plaque formation and lumen narrowing. It is an inflammatory response of the tissue caused by disruptions in the vessel wall nourishment. Blood vessels are nourished by nutrients originating from the blood of the lumen. In medium-sized and larger vessels, nutrients are additionally provided from outside through a network of capillaries called vasa vasorum. It has recently been hypothesized (Haverich in Circulation 135:205–207, 2017) that the root of atherosclerotic diseases is the malfunction of the vasa vasorum. This, so-called outside-in theory, is supported by a recently developed numerical model (Soleimani et al. in Arch Comput Methods Eng 28:4263–4282, 2021) accounting for the inflammation initiation in the adventitial layer of the blood vessel. Building on the previous findings, this work proposes an extended material model for atherosclerosis formation that is based on the outside-in theory. Beside the description of growth kinematics and nutrient diffusion, the roles of monocytes, macrophages, foam cells, smooth muscle cells and collagen are accounted for in a nonlinear continuum mechanics framework. Cells are activated due to a lack of vessel wall nourishment and proliferate, migrate, differentiate and synthesize collagen, leading to the formation of a plaque. Numerical studies show that the onset of atherosclerosis can qualitatively be reproduced and back the new theory.
KW - Atherosclerosis
KW - Finite element method
KW - Mechanobiology
KW - Outside-in theory
UR - http://www.scopus.com/inward/record.url?scp=85180474821&partnerID=8YFLogxK
U2 - 10.1007/s10237-023-01790-7
DO - 10.1007/s10237-023-01790-7
M3 - Article
AN - SCOPUS:85180474821
VL - 23
SP - 539
EP - 552
JO - Biomechanics and Modeling in Mechanobiology
JF - Biomechanics and Modeling in Mechanobiology
SN - 1617-7959
IS - 2
ER -