ReviewCoronary artery disease2016
The role of HDL in plaque stabilization and regression: basic mechanisms and clinical implications.
Review in Coronary artery disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 22 citations in OpenAlex.
- Associations of the Monocyte to High-Density Lipoprotein Cholesterol Ratio With Stroke Prevalence and All-Cause Mortality: Evidence From a Population-Based Study.Brain and behavior · 2025Article
- The Role of Lipids in Atherosclerosis: Focus on Molecular Biology Mechanisms and Therapeutic Approaches.Current medicinal chemistry · 2025Review
- Diagnostic Methods of Atherosclerotic Plaque and the Assessment of Its Prognostic Significance-A Narrative Review.Journal of cardiovascular development and disease · 2024Review
- Risk of Ischemic Stroke in Relation toGut and liver · 2024Observational
- The Effectiveness and Safety of Intensive Lipid-Lowering with Different Rosuvastatin-Based Regimens in Patients at High Cardiovascular Disease Risk: A Nonblind, Randomized, Controlled Trial.Reviews in cardiovascular medicine · 2023Article
- HDL-Based Therapy: Vascular Protection at All Stages.Biomedicines · 2023Review
- Apolipoproteins as potential communicators play an essential role in the pathogenesis and treatment of early atherosclerosis.International journal of biological sciences · 2023Review
- On the Aggregation of Apolipoprotein A-I.International journal of molecular sciences · 2022Article
- Intestinal and Hepatic Uptake of Dietary Peroxidized Lipids and Their Decomposition Products, and Their Subsequent Effects on Apolipoprotein A1 and Paraoxonase1.Antioxidants (Basel, Switzerland) · 2021Article
- Monocyte/High-Density Lipoprotein Ratio Predicts the Prognosis of Large Artery Atherosclerosis Ischemic Stroke.Frontiers in neurology · 2021Article
- Biomarker Discovery in Atherosclerotic Diseases Using Quantitative Nuclear Magnetic Resonance Metabolomics.Frontiers in cardiovascular medicine · 2021Review
- Regional Variation in Genetic Control of Atherosclerosis in Hyperlipidemic Mice.G3 (Bethesda, Md.) · 2020Article
- Carotid and Femoral Atherosclerotic Plaques in Asymptomatic and Non-Treated Subjects: Cardiovascular Risk Factors, 10-Years Risk Scores, and Lipid Ratios´ Capability to Detect Plaque Presence, Burden, Fibro-Lipid Composition and Geometry.Journal of cardiovascular development and disease · 2020Article
- What We Have Learned from the Recent Meta-analyses on Diagnostic Methods for Atherosclerotic Plaque Regression.Current atherosclerosis reports · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
On the basis of studies that extend back to the early 1900s, regression and stabilization of atherosclerosis in humans has progressed from being a concept to one that is achievable. Successful attempts at regression generally applied robust measures to improve plasma lipoprotein profiles. Possible mechanisms responsible for lesion shrinkage include decreased retention of atherogenic apolipoprotein B within the arterial wall, efflux of cholesterol and other toxic lipids from plaques, emigration of lesional foam cells out of the arterial wall, and influx of healthy phagocytes that remove necrotic debris as well as other components of the plaque. Currently available clinical agents, however, still fail to stop most cardiovascular events. For years, HDL has been considered the 'good cholesterol.' Clinical intervention studies to causally link plasma HDL-C levels to decreased progression or to the regression of atherosclerotic plaques are relatively few because of the lack of therapeutic agents that can selectively and potently increase HDL-C. The negative results of studies that were carried out have led to uncertainty as to the role that HDL plays in atherosclerosis. It is becoming clearer, however, that HDL function rather than quantity is most crucial and, therefore, discovery of agents that enhance the quality of HDL should be the goal.
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.