ArticleFrontiers in cardiovascular medicine2025
Investigating the impact of microcalcification size and volume on collagenous matrix and tissue mechanics using a tissue-engineered atherosclerotic cap model.
Article in Frontiers in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Microcalcification: Effects on Atherosclerotic Vulnerable Plaques, Detection, and Therapeutic Perspectives.Current atherosclerosis reports · 2026Review
- Biomechanics of Plaque Rupture and Cardiovascular Calcification.Advances in experimental medicine and biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerotic plaque rupture can lead to thrombotic cardiovascular events such as stroke and myocardial infarction. Computational models have shown that microcalcifications (calcified particles with a diameter < 50 μm) in the atherosclerotic plaque cap can increase cap tissue stresses and consequently contribute to plaque rupture. Microcalcification characteristics, such as particle size and volume fraction, have been implicated to affect cap stresses. However, the effect of these characteristics on tissue mechanics within a collagenous matrix, has not been investigated experimentally. In this study, we employ a tissue-engineered model of the atherosclerotic plaque cap with human myofibroblasts to assess the impact of microcalcification size and volume fraction on cap mechanics and rupture. To mimic human microcalcification size and volume, hydroxyapatite microparticles, in two size ranges (diameter up to 5 μm or up to 50 μm) and two volumes (1 v/v% and 5 v/v%) were incorporated homogenously throughout the tissue-engineered model. 5 v/v% of particles caused a significant lowering of the mechanical properties as was shown by a decrease in stiffness and ultimate tensile stress under uniaxial tensile loading. Additionally, the 5 v/v% of hydroxyapatite particles, in both size ranges, caused a reduced tissue compaction during culture. This might indicate that hydroxyapatite particles influence mechanobiological processes governing tissue organisation and consequent tissue mechanics. These experimental data support computational findings regarding the detrimental role of microcalcifications on cap rupture risk and highlight the importance of volume fraction. Furthermore, this study indicates an additional importance to look at the interplay between calcification, its effect on plaque cap-resident cells and the consequent effect on tissue mechanics.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.