Evidence map›Paper›PMID 40929301›Full record

ArticlePLoS computational biology2025

In silico biophysics and rheology of blood and red blood cells in Gaucher Disease.

Zhaojie Chai, Guansheng Li, Papa Alioune Ndour, Philippe Connes, Pierre A Buffet, Melanie Franco, George Em Karniadakis

Abstract read
In one paragraph

Article in PLoS computational biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

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0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Zhaojie ChaiDivision of Applied Mathematics, Brown University, Providence, Rhode Island, United States of America.ORCID 0000-0001-6571-247X
Guansheng LiDivision of Applied Mathematics, Brown University, Providence, Rhode Island, United States of America.
Papa Alioune NdourUniversité Paris-Cité, INSERM, EFS, BIGR U1134, Paris, France.
Philippe ConnesUniversity Lyon, LIBM EA7424, Vascular Biology and Red Blood Cell Team, Universite Lyon 1, Villeurbanne, France.
Pierre A BuffetUniversité Paris-Cité, INSERM, EFS, BIGR U1134, Paris, France.
Melanie FrancoUniversité Paris-Cité, INSERM, EFS, BIGR U1134, Paris, France.
George Em KarniadakisDivision of Applied Mathematics, Brown University, Providence, Rhode Island, United States of America.ORCID 0000-0002-9713-7120

Funding

Multifidelity and multiscale modeling of the spleen function in sickle cell disease with in vitro, ex vivo and in vivo validationsR01HL154150 · NHLBI · BROWN UNIVERSITY · PI Pierre BUFFET, Ming Dao · 2020 to 2026
$3.9M
NHLBI NIH HHS R01 HL154150
6 · The paper itself

Abstract

Gaucher Disease (GD) is a rare genetic disorder characterized by a deficiency in the enzyme glucocerebrosidase, leading to the accumulation of glucosylceramide in various cells, including red blood cells (RBCs). This accumulation results in altered biomechanical properties and rheological behavior of RBCs, which may play an important role in blood rheology and the development of bone infarcts, avascular necrosis (AVN) and other bone diseases associated with GD. In this study, dissipative particle dynamics (DPD) simulations are employed to investigate the biomechanics and rheology of blood and RBCs in GD under various flow conditions. The model incorporates the unique characteristics of GD RBCs, such as decreased deformability and increased aggregation properties, and aims to capture the resulting changes in RBC biophysics and blood viscosity. This study is the first to explore the Young's modulus and aggregation parameters of GD RBCs by validating simulations with confocal imaging and experimental RBC disaggregation thresholds. Through in silico simulations, we examine the impact of hematocrit, RBC disaggregation threshold, and cell stiffness on blood viscosity in GD. The results reveal three distinct domains of GD blood viscosity based on shear rate: the aggregation domain, where the RBC disaggregation threshold predominantly influences blood viscosity; the transition area, where both RBC aggregation and stiffness impact on blood viscosity; and the stiffness domain, where the stiffness of RBCs emerges as the primary determinant of blood viscosity. By analyzing RBC mechanical properties and blood viscosity in relation to bone disease, we find that the RBC aggregation properties, deformability, and blood viscosity, may contribute to its onset. These findings enhance our understanding of how changes in RBC properties impact on blood viscosity and may affect bone health, offering a partial explanation for the bone complications observed in GD patients.

Indexed as

ErythrocytesGaucher DiseaseBiomechanical PhenomenaBlood ViscosityComputational BiologyComputer SimulationElastic ModulusErythrocyte AggregationHemorheologyHumansRheology

Identifiers

PMID40929301
PMCPMC12435781

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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.