ArticlePloS one2016
Atherosclerosis Alters Loading-Induced Arterial Damage: Implications for Robotic Surgery.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Aerobic exercise-induced irisin secretion is associated with improved endothelial function and reduced atherosclerosis in ApoE-deficient mice.Scientific reports · 2026Article
- Aerobic Exercise Restores Aging-Associated Reductions in Arterial Adropin Levels and Improves Adropin-Induced Nitric Oxide-Dependent Vasorelaxation.Journal of the American Heart Association · 2021Article
- A Chemomechanobiological Model of the Long-Term Healing Response of Arterial Tissue to a Clamping Injury.Frontiers in bioengineering and biotechnology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLack of intra-operative haptic information during robotic surgery increases the risk for unintended tissue overload and damage. Knowledge about the acute and chronic fundamental relationship between force load and induced damage in healthy and diseased arteries is crucial to enable intra-operative haptic feedback or shared autonomy and improve patient safety.
methodsArteries of wildtype and atherosclerotic mice were clamped in vivo for 2 minutes (0.0N, 0.6N or 1.27N). Histological analysis (Verhoeff's-Van Gieson, Osteopontin, CD45, CD105) was performed immediately, or after 6 hours, 2 weeks or 1 month. Endothelium-dependent and-independent vasodilatation was assessed immediately or 1 month after clamping.
resultsEndothelium dependent vasodilatation is worse after clamping of wildtype arteries, but is restored after one month. Clamping also results in flattening of the innermost elastic membrane of both genotypes, which is reversed over time for wildtype arteries but not for vessels from atherosclerotic mice. Higher osteopontin content in wildtype and LDLR-/- mice after 2 weeks suggests a phenotypic switch of the medial smooth muscle cells (SMCs), an effect that is reversed after 1 month. While inflammation in the intima diminishes, medial CD45 content rises through time in both genotypes. CD105 staining shows that even manipulation without clamping results in endothelial cell loss in both LDLR+/+ and LDLR-/- mice.
conclusionsArterial clamping induces different acute and long-term injury to the vessel wall of atherosclerotic and healthy arteries.
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.