ArticleJournal of lipid research2009
Molecular and cellular mechanisms of the thrombotic complications of atherosclerosis.
Article in Journal of lipid research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 2 of them syntheses that pooled it.
What it found
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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.
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Who cites it
49 citing papers in PubMed, 2 syntheses or guidelines pooled it, 139 citations in OpenAlex.
- Pooled it
- Pooled it
- Apolipoprotein B in cardiovascular risk assessment: beyond traditional lipid markers.Frontiers in cardiovascular medicine · 2026Review
- Evaluation of tissue-engineered blood vessels as three-dimensional in vitro testing system in cardiovascular research.Frontiers in bioengineering and biotechnology · 2026Article
- Elevated inflammatory index and future risk of stroke in patients with coronary heart disease: a multicenter prospective cohort study.Frontiers in cardiovascular medicine · 2025Article
- Atherosclerosis: from lipid-lowering and anti-inflammatory therapies to targeting arterial retention of ApoB-containing lipoproteins.Frontiers in immunology · 2025Review
- Circulating mitochondrial biomarkers in acute coronary syndrome.Frontiers in medicine · 2025Article
- Evaluation of Cognitive Functions in Patients with Acute Coronary Syndrome Undergoing Percutaneous Coronary Intervention: A Prospective Pilot Study.Diagnostics (Basel, Switzerland) · 2024Article
- Stroke risk in rheumatoid arthritis patients: exploring connections and implications for patient care.Clinical and experimental medicine · 2024Review
- Regulation of toll-like receptor (TLR) signaling pathways in atherosclerosis: from mechanisms to targeted therapeutics.Acta pharmacologica Sinica · 2023Review
- Advances in treatment strategies based on scavenging reactive oxygen species of nanoparticles for atherosclerosis.Journal of nanobiotechnology · 2023Review
- Anti-Atherogenic Protection by Oligomeric Proanthocyanidins via Regulating Collagen Crosslinking Against CC Diet-Induced Atherosclerosis in Rats.Applied biochemistry and biotechnology · 2023Article
- Causal relationship between spondylarthritis and stroke in a European population: a two sample Mendelian randomization study.Frontiers in immunology · 2023Article
- Assessment and Mitigation of Cardiovascular Risk for Prostate Cancer Patients: A Review of the Evidence.International journal of clinical practice · 2022Review
- Inflammation, Oxidative Stress, Senescence in Atherosclerosis: Thioredoxine-1 as an Emerging Therapeutic Target.International journal of molecular sciences · 2021Review
- Lab-on-a-Chip for Cardiovascular Physiology and Pathology.Micromachines · 2020Review
- CCL4 Inhibition in Atherosclerosis: Effects on Plaque Stability, Endothelial Cell Adhesiveness, and Macrophages Activation.International journal of molecular sciences · 2020Article
- Oxidized Low-Density Lipoprotein Induces Macrophage Production of Prothrombotic Microparticles.Journal of the American Heart Association · 2020Article
- Review
- Activation of immune responses against the basement membrane component collagen type IV does not affect the development of atherosclerosis in ApoE-deficient mice.Scientific reports · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clinicians have traditionally regarded the complications of atherosclerosis as a consequence of progressive arterial stenosis leading to critical narrowings that impede blood flow. Our contemporary understanding of the thrombotic complications of atherosclerosis has undergone a transformation based on a body of observations by pathologists and clinicians. In the late 1980s, clinicians had to confront the counterintuitive notion that plaques that cause acute myocardial infarction often do not produce high-grade stenoses (Smith, S. C., Jr. 1996. Risk-reduction therapy: the challenge to change. Circulation. 93: 2205-2211.). Observations from serial angiographic studies and on culprit lesions of acute myocardial infarction postthrombolysis highlighted this apparent paradox. These contrarian clinical findings prompted cardiologists to consider more carefully the findings of generations of pathologists that plaques that cause fatal coronary thrombi often result from a physical disruption of the atheromatous plaque that may not indeed cause critical arterial narrowing. This convergence of clinical and pathological observations highlighted the importance of understanding the mechanisms of disruption of plaques that can precipitate thromboses.
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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.