ReviewArteriosclerosis, thrombosis, and vascular biology2025
Atherosclerotic Plaque Instability and Rupture: Recommended Mouse Models to Empower Clinically Relevant Discoveries, Diagnostics, and Therapeutics.
Review in Arteriosclerosis, thrombosis, and vascular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed.
- Impaired Glycolysis Leads to Defective Efferocytosis and Impaired Plaque Resolution inCirculation · 2026Article
- Plaque-Hepatic Targeting Nanotherapy Disrupts the PCSK9-LOX-1 Axis to Suppress oxLDL in Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Heparanase gene deficiency suppresses atherosclerosis progression and enhances plaque stability in apolipoprotein E gene knockout mice with diabetes.Clinical science (London, England : 1979) · 2026Article
- Mouse Models of Atherosclerosis: What They Teach Us, What They Miss, and When to Use Them.Bioengineering (Basel, Switzerland) · 2026Review
- Rethinking the selection of in vivo thrombosis models in the hybrid era.Nature cardiovascular research · 2026Article
- Monocyte Chemokines Enhance Atherosclerotic Plaque Necrosis After Bacterial Kidney Infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- P-Selectin and Platelet-Monocyte Interaction in Inflammation: Mechanisms, Hypothesis, and Open Questions.Journal of inflammation research · 2026Review
- Sex-specific lymphatic responses to estrogen shape atherosclerosis in high-risk mice.Frontiers in cardiovascular medicine · 2026Article
- The possible mechanisms linking chronic obstructive pulmonary disease and coronary atherosclerosis based on coronary computed tomography angiography and animal experiments.Frontiers in physiology · 2026Article
- Mechanisms of Yiqi Huoxue Granule in Atherosclerosis Treatment: Insights from UPLC-Q-Exactive Orbitrap-MS Analysis, Network Pharmacology, Molecular Docking, and Experimental Verification.Journal of inflammation research · 2026Article
- Unmasking the haemostatic potential of quotidian plastics: upon first glance.Frontiers in pharmacology · 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
4 authors.
Funding
Abstract
clinical problemAtherosclerotic plaque instability/rupture is the major driver of myocardial infarction and stroke, the leading causes of cardiovascular morbidity/mortality. However, the mechanisms leading to plaque rupture are poorly understood. This limits our ability to establish sensitive and diagnostic tools to identify plaques that are prone to rupture and to develop much-needed plaque-stabilizing therapies. RECOMMENDATIONS: The diagnostic identification and therapeutic stabilization of unstable plaques are considered the holy grail of cardiovascular medicine, holding the potential to significantly reduce cardiovascular morbidity/mortality. To achieve this, it is vital that preclinical models reflect plaque instability/rupture as observed in patients. This will allow mechanistic discoveries, the development of diagnostic tools, and treatment options to identify and stabilize rupture-prone, unstable atherosclerotic plaques. This can be achieved using appropriate, research question-dependent, but currently underutilized mouse models with direct translational relevance. SUMMARY OF STRENGTHS AND WEAKNESSES OF MOUSE MODELS FOR ATHEROSCLEROSIS: Conventional mouse models of atherosclerosis, LDLR
Indexed as
Identifiers
What Socratic 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 Socratic graph.