Evidence map›Paper›PMID 42149930›Full record

ArticlePLoS computational biology2026

Multiscale modeling of blood circulation with cerebral autoregulation and network pathway analysis for hemodynamic redistribution in the vascular network with anatomical variations and stenosis conditions.

Jiawei Liu, Atsushi Kanoke, Hidenori Endo, Kuniyasu Niizuma, Hiroshi Suito

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Article in PLoS computational biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Jiawei LiuAdvanced Institute for Materials Research, Tohoku University, Sendai, Japan.ORCID https://orcid.org/0000-0002-0852-4779
Atsushi KanokeDepartment of Neurosurgery, Kohnan Hospital, Sendai, Japan.
Hidenori EndoDepartment of Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Japan.
Kuniyasu NiizumaDepartment of Translational Neuroscience, Tohoku University Graduate School of Medicine, Sendai, Japan.
Hiroshi SuitoAdvanced Institute for Materials Research, Tohoku University, Sendai, Japan.ORCID https://orcid.org/0000-0003-2043-3527

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral hemodynamics is fundamentally regulated through the Circle of Willis (CoW), which redistribute flow via communicating arteries to stabilize perfusion under anatomical variations and vascular stenosis. In this study, a multiscale circulation model was developed by coupling a multiscale systemic hemodynamic framework with cerebral arterial network reconstructed from medical imaging. The model integrates a cerebral autoregulation mechanism (CAM) and enables quantitative simulation of flow redistribution across the CoW under normal, anatomically varied, and pathologically narrowing (stenosis) conditions. Baseline simulations at normal states reproduced physiological flow distributions in which the communicating arteries remained nearly inactive, showing negligible across-flow and agreement with clinical measurements, while two anatomical variations revealed distinct collateral activation patterns: the anterior communicating artery (ACoA) acted as the earliest and most sensitive functional collateral pathway, whereas the posterior communicating arteries (PCoAs) exhibited structure-dependent engagement. Progressive stenosis modeling further demonstrated the transition from a complete CoW to a fetal-type posterior cerebral artery (PCA) configuration, with early ACoA flow reversal followed by the ipsilateral PCoA activation, in agreement with experimental and transcranial Doppler observations. We further present a path-based quantitative analysis of source-to-sink flow contributions to quantitatively illustrates how the cerebral vascular network dynamically reconfigures collateral pathways in response to structural changes. Overall, the proposed framework provides a physiologically interpretable and image-informed tool for investigating cerebral flow regulations through the functional collaterals within the CoW, offering potential for clinical applications in the diagnosis, prognosis, and treatment planning of cerebrovascular diseases.

Indexed as

Cerebrovascular CirculationHemodynamicsModels, CardiovascularAnimalsBlood Flow VelocityCerebral ArteriesCircle of WillisComputer SimulationConstriction, PathologicHomeostasisHumans

Identifiers

PMID42149930
PMCPMC13211260

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.