Evidence map›Paper›PMID 39949493›Full record

ArticleCellular and molecular bioengineering2025

Theoretical and Experimental Studies of the Dynamic Damage of Endothelial Cellular Networks Under Ultrasound Cavitation.

Chuangjian Xia, Jiwen Hu, Kun Zhou, Yingjie Li, Sha Yuan, Qinlin Li

Abstract read
In one paragraph

Article in Cellular and molecular bioengineering, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Chuangjian XiaSchool of Mathematics and Physics, University of South China, Hengyang, 421001 China.
Jiwen HuSchool of Mathematics and Physics, University of South China, Hengyang, 421001 China.ORCID 0000-0003-1930-0188
Kun ZhouHengyang Medical School, University of South China, Hengyang, 421001 China.
Yingjie LiSchool of Mathematics and Physics, University of South China, Hengyang, 421001 China.
Sha YuanSchool of Mathematics and Physics, University of South China, Hengyang, 421001 China.
Qinlin LiSchool of Mathematics and Physics, University of South China, Hengyang, 421001 China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: The interaction between endothelial cells can regulate hemostasis, vasodilation, as well as immune and inflammatory responses. Excessive loading on the endothelial cells leads to endothelial damage and endothelial barrier dysfunction. Understanding and mastering the dynamic nature of cell-cell rupture plays a crucial role in exploring the practical applications related to tumor destruction, vascular remodeling, and drug delivery by employing cavitation-induced damage to soft tissues. Methods: To investigate the damage mechanisms of endothelial cellular networks under ultrasound cavitation, we developed a model of junction rupture in cellular networks based on the assumption that the process of intercellular rupture is irreversible when ultrasound-mediated forces exceed the damage threshold, whereas intercellular junctions have reversible behavior before rupture. Simulations using the strain accumulation method show that stress and strain exhibit complex nonlinear dynamic behavior. Ultrasonic cavitation damage was tested and evaluated on human umbilical vein endothelial cells. Results: The results indicated that the cellular network damage was positively correlated with force amplitude and pulse frequency and was negatively correlated with driving frequency. The time lag and the internal force of cellular junctions have an important influence on the resistance to damage of the cellular network due to external forces. The damage experiment based on ultrasonic cavitation confirmed the effectiveness of the proposed model. Conclusions: The model provided a platform for understanding the damage mechanism of endothelial tissues and ultimately improving options for their prevention and treatment.

Indexed as

Cavitation damageCell–cell ruptureEndothelial cellsIntercellular junctions

Identifiers

PMID39949493
PMCPMC11813858

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