Biomechanics and Modeling in Mechanobiology最新文献

{"title":"Lumped parameter modeling of changes in liver hemodynamics due to cirrhosis","authors":"Edith Luveina Joseph,&nbsp;Himanshi Saini,&nbsp;Usha Kini,&nbsp;Timothy L. Pruett,&nbsp;Joseph Sushil Rao,&nbsp;Jeffrey Tithof","doi":"10.1007/s10237-026-02055-9","DOIUrl":"10.1007/s10237-026-02055-9","url":null,"abstract":"<div><p>This numerical study employs a computational model of human hepatic blood flow to investigate the hemodynamic consequences of cirrhosis. The liver receives blood through a dual-inlet system (portal vein and hepatic artery) that perfuses a complex network of sinusoids; however, cirrhosis-induced fibrosis distorts these channels, increasing hydraulic resistance. In turn, portal pressure is elevated, leading to the potential recanalization of portosystemic collaterals. We extended a lumped parameter hydraulic network model of the human liver, with demarcation of Couinaud segments, to capture the effects of fibrosis by incorporating a portosystemic collateral pathway and an “apparent viscosity” formulation that accounts for the non-Newtonian properties of blood. Our simulations indicate that segment-wise reductions in mean sinusoid conductance, combined with increased heterogeneity, drive the flow redistribution characteristic of the clinical “atrophy-hypertrophy complex”. This results in diminished perfusion and wall shear stress in right-lobe segments, while flow and wall shear stress is preserved or even elevated in the left lobe. Sensitivity analysis suggests that the onset of portal hypertension is driven primarily by the reduction of mean sinusoid conductance, not increased heterogeneity. However, increased heterogeneity likely exacerbates liver dysfunction, as the model predicts that a disproportionately large fraction of blood passes through the relatively few sinusoids with the lowest hydraulic resistance. Additionally, results demonstrate that while the dilatation of portosystemic collaterals effectively offloads the portal system, it leads to a substantial increase in overall blood flow, contributing to hyperdynamic circulation (a hallmark feature of cirrhosis). These predictions provide quantitative, mechanistic insights into the hemodynamic and anatomical alterations of cirrhosis, offering a computational framework that helps explain clinical observations and may assist in future patient-specific surgical planning.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10237-026-02055-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147986073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Computational hemodynamic analysis of renal blood flow and the impact of outflow boundary conditions","authors":"Fenfen Qi,&nbsp;Yingzhi Liu,&nbsp;Rongliang Chen,&nbsp;Xiao-Chuan Cai","doi":"10.1007/s10237-026-02065-7","DOIUrl":"10.1007/s10237-026-02065-7","url":null,"abstract":"<div><p>Hemodynamic analysis is an essential tool for predicting the behavior of blood flows and assessing the risk of renovascular diseases. In this paper, by employing a CFD-based finite element method coupled with an efficient parallel algorithm for the unsteady incompressible Navier–Stokes equations, we conduct a comprehensive investigation of renal hemodynamics and the impact of outflow boundary conditions in patient-specific models of normal, stenotic, and aneurysmal arteries featuring rich small-branch networks. Based on the hemodynamic analysis for the severe stenosis (area stenosis <span>(&gt;87%)</span>) and the aneurysm (diameter <span>(=13.3)</span> mm), we observe a pressure drop exceeding 10 mmHg and a distal-to-proximal pressure ratio below 0.9 for these lesions, which is considered hemodynamically significant and likely induces renovascular hypertension. Furthermore, we reveal that the low wall shear stress and complex vortices with bidirectional flow occur on the inner wall downstream of this stenosis, which play a critical role in driving atherosclerotic plaque formation. Through virtual aneurysm reconstruction and numerical simulation, we demonstrate that the presence of a renal aneurysm alters local flow patterns and pressure distributions. Numerical results for both healthy and pathological renal arteries show that outflow boundary conditions have a significant impact on the global distribution of pressure and local flow patterns near the outlets. Compared with constant pressure and resistance outflow boundary conditions, the two-element Windkessel model, through adjustments of its resistance and capacitance parameters, can provide more physiological flow and pressure distributions, particularly in capturing realistic pulsatile waveforms, pressure ranges, and distal flow patterns. Moreover, a sensitivity analysis of the resistance in the Windkessel boundary condition shows a negligible impact on the pressure drop and only a minor effect on the renal fractional flow reserve (a change of less than <span>(3%)</span> for a <span>(20%)</span> variation in resistance). When focusing solely on the hemodynamics within stenotic and aneurysmal lesions located far from the outlets, both the constant pressure and Windkessel boundary conditions yield comparable results for key lesion-specific hemodynamic indicators, including renal fractional flow reserve and pressure drop in the stenosis, and wall shear stress and oscillatory shear index in the aneurysm.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147985984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Longitudinal associations between hemodynamic surrogate measures and morphological progression in abdominal aortic aneurysm","authors":"MyeungHye Suh,&nbsp;Up Huh,&nbsp;Chiseung Lee","doi":"10.1007/s10237-026-02079-1","DOIUrl":"10.1007/s10237-026-02079-1","url":null,"abstract":"<div><p>Abdominal aortic aneurysm (AAA) is often asymptomatic, making early detection challenging. As the aneurysm expands, it alters the hemodynamic forces exerted on the arterial wall, which in turn influence disease progression. This study investigated longitudinal association between geometric structure and hemodynamics, along with changes in maximum diameter, volume, total surface area, and aneurysm sac surface area, using a longitudinal dataset of 36 computed tomography angiography (CTA) scans collected from eight patients over multiple time points. Hemodynamic parameters—including time-averaged wall shear stress (TAWSS), oscillatory shear index (OSI), relative residence time (RRT), endothelial cell activation potential (ECAP), velocity shear rate, and pressure—were derived via computational fluid dynamics (CFD) simulations. These parameters were analyzed alongside geometric indices such as the asymmetry index, saccular index, tortuosity index, and deformation diameter ratio. To account for the longitudinal nature of the data and inter-patient heterogeneity, a linear mixed model (LMM) was employed for the statistical analysis. Results revealed that across the AAA region, TAWSS and <span>(dot{v})</span> _mean decreased significantly during aneurysm expansion, while ECAP and pressure showed strong positive associations with marginal <span>({R}^{2})</span> values exceeding 0.9 (e.g., ECAP_max <span>({R}^{2})</span>= 0.977; Pressure_max <span>({R}^{2})</span>= 0.979). Geometric factors like the saccular index and deformation diameter ratio also strongly associated with aneurysm growth (<span>({R}^{2})</span>&gt; 0.94), whereas the asymmetry index showed no significant relationship. These findings suggest that longitudinal associations exist between aneurysm morphology and CFD-derived hemodynamic surrogate measures, providing complementary descriptive information alongside conventional morphology-based assessment.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147986031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reducing descending aortic tortuosity improves thoracic endovascular aortic repair outcomes in type B aortic dissection: from a hemodynamic perspective","authors":"Yue Che,&nbsp;Yining Zhang,&nbsp;Jiawei Zhao,&nbsp;Fei Liu,&nbsp;Puyi Zhao,&nbsp;Jing Zhu,&nbsp;Xuelan Zhang,&nbsp;Chang Shu,&nbsp;Mingyao Luo","doi":"10.1007/s10237-026-02066-6","DOIUrl":"10.1007/s10237-026-02066-6","url":null,"abstract":"<div><p>For patients with tortuous descending aortas undergoing thoracic endovascular aortic repair (TEVAR), reducing tortuosity may optimize stent-wall conformity and improve surgical outcomes, but its necessity remains unclear. This study aims to verify the necessity of reducing descending aortic tortuosity while sealing the tears during TEVAR for type B aortic dissection (TBAD) patients from a hemodynamic perspective. Radiological imaging data (pre- and post-TEVAR) of nine TBAD patients with tortuous descending aortas were collected, and subject-specific aortic geometries were reconstructed. Meanwhile, virtual TEVAR geometries with pre-TEVAR tortuosity were created as a control group for post-TEVAR. Computational fluid dynamics simulations were conducted and hemodynamic indicators were comparatively analyzed by statistics among three groups, including vorticity, displacement force, time-averaged wall shear stress (TAWSS), oscillatory shear index (OSI) and relative residence time (RRT). Compared to pre-TEVAR, the hemodynamic indicators of the post-TEVAR group improved significantly (<i>p</i> &lt; 0.050), while those in the virtual TEVAR group were not significant (<i>p</i> &gt; 0.050). The post- and virtual TEVAR group exhibited improvements to pre-TEVAR in vorticity (36.44% vs. 27.10%), displacement force (14.51% vs. 4.77%), TAWSS (57.06% vs. 10.90%), OSI (27.24% vs. 6.03%) and RRT (48.58% vs. 16.74%), respectively. Additionally, the left subclavian artery perfusion in post-TEVAR increased by 58.73% compared with pre-TEVAR (<i>p</i> = 0.022), significantly more than the 22.68% increase (<i>p</i> = 0.175) in the virtual group. Reducing descending aortic tortuosity during TEVAR yields significant hemodynamic benefits. This may potentially enhance graft stability and promote long-term TEVAR efficacy.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147969480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A mathematical model of osteocyte network control of bone mechanical adaptation","authors":"Adel Mehrpooya,&nbsp;Vivien J. Challis,&nbsp;Pascal R. Buenzli","doi":"10.1007/s10237-026-02069-3","DOIUrl":"10.1007/s10237-026-02069-3","url":null,"abstract":"<div><p>The osteocyte network embedded in bone tissues plays a central role in the control of bone adaptation to mechanical loads and micro-damage repair. However, much remains to be understood about the precise mechanisms by which the osteocyte network regulates bone formation and bone resorption based on the propagation of biochemical signals emitted in response to mechanical stimulus. In this work, we propose a one-dimensional computational model of bone mechanical adaptation based on the propagation of signalling molecules through a dynamic osteocyte network. The osteocyte network is extended during bone formation and reduced during bone resorption, which affects the generation and propagation of the signalling molecules to the bone surface. We explore how this osteocyte-based model of bone mechanosensation and mechanoresponse gives rise to effective Wolff’s laws, in which overloaded bone is consolidated and underloaded bone is removed. We find that the discrete addition and removal of osteocytes significantly affects signalling molecules propagating to the bone surface and leads to new bone adaptation behaviours compared to earlier models, including partial bone recovery following an unloading and reloading cycle and the emergence of a minimum threshold of mechanical stress below which all bone is resorbed. While many extensions of this mathematical model are possible, it provides a first illustration of how the osteocyte network could act as a dynamic embedded control network for bone adaptation to mechanical loads.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13160984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147872992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms driving thoracic aortic aneurysm instability","authors":"Erica L. Schwarz,&nbsp;David S. Li,&nbsp;Colin W. Means,&nbsp;Roland Assi,&nbsp;Jay D. Humphrey","doi":"10.1007/s10237-026-02054-w","DOIUrl":"10.1007/s10237-026-02054-w","url":null,"abstract":"<div><p>Thoracic aortic aneurysms arise from a combination of biological and mechanical factors. Current clinical guidelines use size and rate of expansion to stratify risk, but such metrics do not necessarily predict if an aneurysm will stabilize, grow, dissect, or rupture. Computational biomechanical models can provide additional insights into mechanisms of aneurysm behavior that would be difficult or impossible to capture in vivo. Here, we use a constrained mixture theory of growth and remodeling to simulate lesion progression while covarying rate-dependent parameters that contribute to the natural history of aneurysm growth. This includes insults to the material properties of the vascular wall and the sensitivity of the vascular cells to their mechanical environment. This framework successfully simulates clinically relevant phenotypes, including cases where lesions with initially similar degrees of dilatation or rates of expansion diverge in behavior later in their progression. By capturing this spectrum of outcomes, our framework lays a foundation for more accurate, patient-specific risk prediction and future integration of machine learning tools to accelerate translation into clinical practice.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147866310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the fluid mechanical mechanisms of sound production in pulsatile tinnitus using high-fidelity CFD","authors":"Anna L. Haley,&nbsp;Gurnish Sidora,&nbsp;Nicole M. Cancelliere,&nbsp;Vitor M. Pereira,&nbsp;David A. Steinman","doi":"10.1007/s10237-026-02049-7","DOIUrl":"10.1007/s10237-026-02049-7","url":null,"abstract":"<div><p>Venous pulsatile tinnitus (PT) is sound associated with abnormal blood flow near auditory structures in the head, which can impact mental health and may be associated with intracranial hypertension. High-frequency flow instabilities, vortical flow, and regions of high time-averaged wall shear stress (TAWSS) have previously been associated with the sounds of PT, but do not identify potential mechanisms for sound production. In this study, the spectral power index of the wall pressure (<span>(textrm{SPI}_{P})</span>) was used to determine the locations where sound could be transmitted through the walls of cerebral venous sinuses. These locations were then analyzed using maximum dissipation maps, streamlines, spectrograms, and swirling strength to understand the underlying flow phenomena that induce sound production. The results show that regions of high <span>(textrm{SPI}_{P})</span> do not correspond with high TAWSS, vortical flow, or regions of highest dissipation. Rather, they appear to occur beyond regions of high dissipation where part of the post-stenotic flow splits off and interacts with obstructions, forming larger structures that beat against the wall, in addition to smaller flow structures. It is proposed that these structures are capable of producing the intermittency in pressure required to create sound that may be able to transmit to the ear.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147830155","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Coupled mixed-dimensional multiphase porous media approach for modeling airflow, blood flow, and gas exchange in the human lungs","authors":"Lea J. Köglmeier,&nbsp;Barbara Wirthl,&nbsp;Carolin M. Eichinger,&nbsp;Buğrahan Z. Temür,&nbsp;Wolfgang A. Wall","doi":"10.1007/s10237-026-02064-8","DOIUrl":"10.1007/s10237-026-02064-8","url":null,"abstract":"<div><p>Mechanical ventilation is a life-saving therapeutic intervention for patients with impaired pulmonary function, yet it carries the risk of ventilator-induced lung injury (VILI). At bedside, physicians face the challenge of keeping lung tissue in a healthy state while ensuring sufficient gas exchange. Gas exchange occurs between the air in the alveoli and the dense network of pulmonary blood vessels in their walls, and it strongly depends on the balance between ventilation and perfusion. Mismatches between them are a major cause of impaired gas exchange in pulmonary diseases. However, the precise effects of ventilation, including tissue straining on the pulmonary circulation and the connected gas exchange, are largely unknown. Here, we therefore present an approach to computationally model the respiratory and circulatory systems of the human lungs, including gas exchange. Motivated by the lung’s hierarchical structure, our model represents larger airways and blood vessels as spatially resolved discrete networks of zero-dimensional (0D) models that are embedded into a multiphase porous medium (3D). The porous medium models the smaller respiratory and vascular structures, including lung tissue mechanics, in a homogenized way. Additionally, the respiratory gases—oxygen and carbon dioxide—are incorporated as chemical subcomponents of air and blood, with an exchange model in the porous domain. To connect the homogenized (porous domain) and the discrete (networks) representations of airways and blood vessels, we use a 0D-3D coupling method that allows a non-matching spatial discretization of both domains. This comprehensive coupled approach is physics-based, i.e., based on the underlying physical mechanisms, allowing us to investigate the (often unknown and unmeasurable) interplay between ventilation, tissue deformation, perfusion, and its effects on gas exchange dynamics. We anticipate our approach to be an important milestone towards better addressing clinically relevant questions in respiratory care <i>in silico</i>, which will contribute to developing improved ventilation strategies and better patient outcomes.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10237-026-02064-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Homeostatic pressure of a proliferating multicellular foam with hydromechanical volume regulation","authors":"Jef Vangheel,&nbsp;Jeroen Guillierme,&nbsp;Irish Senthilkumar,&nbsp;Enda Howley,&nbsp;Eoin McEvoy,&nbsp;Bart Smeets","doi":"10.1007/s10237-026-02068-4","DOIUrl":"10.1007/s10237-026-02068-4","url":null,"abstract":"<div><p>The dynamics of tumor growth and its competition with host tissue depend not only on proliferation rates but also on the mechanical properties of individual cells. Here, we present a hydromechanical model that couples osmotic volume regulation to tissue mechanics, representing multicellular aggregates as a proliferating foam of interacting cells. In confined conditions, we simulate multicellular growth until reaching a hydromechanical steady-state with a compressive multicellular stress. Next, we show that both increased adhesive tension and reduced surface tension increase the homeostatic pressure of a growing aggregate. This mechanical advantage allows softer and more adhesive cells to outcompete stiffer and even faster-growing populations. Our results demonstrate that single-cell mechanics can override proliferation rate in determining growth dynamics and competitive outcomes in multicellular aggregates.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147738304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In silico analysis of the invasion mechanics and invasiveness of the Plasmodium falciparum merozoite","authors":"Chimwemwe Msosa,&nbsp;Tamer Abdalrahman,&nbsp;Thomas Franz","doi":"10.1007/s10237-026-02062-w","DOIUrl":"10.1007/s10237-026-02062-w","url":null,"abstract":"<div><p>Although there has been considerable progress in understanding the factors that determine the invasiveness of Plasmodium falciparum merozoites, the collective role of the biophysical characteristics of erythrocyte deformability in the invasion process is poorly understood. Cell shape, cytoplasmic viscosity, and membrane stability are the main determinants of erythrocyte deformability, but it remains unknown how these properties affect the merozoite invasiveness. This study aimed to investigate computationally (i) the role of erythrocyte morphology and merozoite-induced erythrocyte membrane damage in merozoite invasion and (ii) the suitability of mechanical markers of merozoite-induced erythrocyte membrane damage for screening of invasion-blocking antimalarial drugs. Finite element models were developed to represent a human erythrocyte and a spherocyte, their invasion by a malaria merozoite, and erythrocyte compression and nanoindentation as mechanical assays for membrane damage. Smoothed particle hydrodynamics represented the erythrocyte cytoplasm, and merozoite-induced erythrocyte membrane damage was implemented with a constitutive model. The invasiveness of the merozoite decreases with increased erythrocyte sphericity associated with genetic disorders such as hereditary spherocytosis. The invasiveness is larger when membrane damage is induced in the erythrocyte at an early invasion stage than throughout the invasion process. The minimum force required for a malaria merozoite to invade a human erythrocyte was predicted to be 11 pN. The findings on the invasion mechanics can guide future studies into the invasiveness of the merozoite. The nanoindentation simulations point to the potential of nanoindentation to determine erythrocyte membrane damage for screening novel invasion-blocking antimalarial drugs.</p></div>","PeriodicalId":489,"journal":{"name":"Biomechanics and Modeling in Mechanobiology","volume":"25 3","pages":""},"PeriodicalIF":2.7,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10237-026-02062-w.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147707787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}