ArticleMechanobiology in medicine2025
Tropomodulin1 regulates the biomechanical changes in macrophages induced by matrix stiffness.
Article in Mechanobiology in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled 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.
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
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Macrophage mechanobiology: from sensing to disease.Frontiers in immunology · 2026Pooled it
- Substrate pre-stretch reprograms macrophage behavior through surface topographical remodeling.Mechanobiology in medicine · 2026Article
- Mechanobiology of intervertebral disc degeneration: From pathological mechanisms to therapeutic approaches.Mechanobiology in medicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The monocyte/macrophage infiltration plays critical roles in the development of atherosclerosis. Arterial stiffness is a cholesterol-independent risk factor for cardiovascular events. The regulation of arterial stiffness on biomechanics of macrophages and its underlying mechanism remains unclear. We prepared polyacrylamide gels with low and high stiffness that corresponded to healthy and diseased blood vessels, respectively. We found that macrophages cultured on stiff matrix had increased rigidity and migration ability compared to those on soft matrix. An actin capping protein, tropomodulin1 (Tmod1) was upregulated in macrophages by stiff matrix and in arteries with high stiffness. Further analyses showed that deficiency of Tmod1 in macrophages completely or partially prevented the changes in actin polymerization, cell adhesion and cell spreading induced by stiff matrix. Overexpression of Tmod1 in macrophages enhanced actin polymerization, cell adhesion and spreading on stiff matrix. Tmod1 was involved in the regulation of vinculin expression and formation of focal adhesion in macrophages on stiff matrix. Finally, the deficiency of Tmod1 in macrophages retarded the formation of atherosclerotic plaques in blood vessels with high matrix stiffness. The results suggest that Tmod1 was a key regulator in macrophage rigidity and migration on stiff substrate. The present work will help us to understand the biomechanical mechanisms for the development of atherosclerosis.
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.