ReviewCurrent atherosclerosis reports2000
Mechanism of action of niacin on lipoprotein metabolism.
Review in Current atherosclerosis reports, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.
- Effects of combination lipid therapy on coronary stenosis progression and clinical cardiovascular events in coronary disease patients with metabolic syndrome: a combined analysis of the Familial Atherosclerosis Treatment Study (FATS), the HDL-Atherosclerosis Treatment Study (HATS), and the Armed Forces Regression Study (AFREGS).The American journal of cardiology · 2009 · on this mapPooled it
- Randomized comparative study of the effects of treatment with once-daily, niacin extended-release/lovastatin and with simvastatin on lipid profile and fibrinolytic parameters in Taiwan.The Kaohsiung journal of medical sciences · 2006Trial
- Salvianolic Acid B Alleviates MAFLD by Targeting PPAR-α: Mechanistic Insights From Network Pharmacology and Lipidomics.Food science & nutrition · 2026Article
- High Concentrations of Circulating 2PY and 4PY-Potential Risk Factor of Cardiovascular Disease in Patients with Chronic Kidney Disease.International journal of molecular sciences · 2025Review
- Exploring the Impact of Niacin Intake on Cardiovascular Outcomes: A Comprehensive Analysis Using NHANES Data (2003-2018).Reviews in cardiovascular medicine · 2024Article
- Niacin promotes the efflux of lysosomal cholesterol from macrophages via the CD38/NAADP signaling pathway.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Systemic vitamin intake impacting tissue proteomes.Nutrition & metabolism · 2020Review
- Niacin regulates apolipoprotein M expression via liver X receptor‑α.Molecular medicine reports · 2019Article
- Determination of niacin profiles in some animal and plant based foods by high performance liquid chromatography: association with healthy nutrition.Journal of animal science and technology · 2019Article
- Role of Nicotinamide Adenine Dinucleotide and Related Precursors as Therapeutic Targets for Age-Related Degenerative Diseases: Rationale, Biochemistry, Pharmacokinetics, and Outcomes.Antioxidants & redox signaling · 2019Review
- Hypertriglyceridemia-Related Pancreatitis In Patients With Type 2 Diabetes: Links And Risks.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019Article
- Review
- Paraoxonase responses to exercise and niacin therapy in men with metabolic syndrome.Redox report : communications in free radical research · 2015Article
- Visceral obesity in normal-weight patients suffering from chronic schizophrenia.BMC psychiatry · 2014Article
- Article
- GPR109A and vascular inflammation.Current atherosclerosis reports · 2013Review
- Nicotinic acid inhibits hepatic APOA gene expression: studies in humans and in transgenic mice.Journal of lipid research · 2012Article
- Niacin in cardiovascular disease: recent preclinical and clinical developments.Arteriosclerosis, thrombosis, and vascular biology · 2012Review
- A review of the rationale for additional therapeutic interventions to attain lower LDL-C when statin therapy is not enough.Current atherosclerosis reports · 2012Review
- Effects of niacin on atherosclerosis and vascular function.Current opinion in cardiology · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is generally accepted that the increased concentrations of apolipoprotein (apo) B containing very low-density lipoproteins (VLDL) and low-density lipoproteins (LDL), and decreased levels of apo AI containing high-density lipoproteins (HDL) are correlated to atherosclerotic cardiovascular disease. Current evidence indicates that the post-translational apo-B degradative processes regulate the hepatic assembly and secretion of VLDL and the subsequent generation of LDL particles. The availability of triglycerides (TG) for the addition to apo B during intracellular processing appears to play a central role in targeting apo B for either intracellular degradation or assembly and secretion as VLDL particles. Based on the availability of TG, the liver secretes either dense TG-poor VLDL2 or large TG-rich VLDL1 particles, and these particles serve as precursors for the formation of more buoyant or small, dense LDL particles by lipid transfer protein- and hepatic lipase-mediated processes. HDLs are a heterogenous class of lipoproteins, and apo AI (the major protein of HDL) participates in reverse cholesterol transport, a process by which excess cholesterol is eliminated. Recent studies indicate that HDL particles containing only apo A-I (LPA-I) are more effective in reverse cholesterol transport and more anti-atherogenic than HDL particles containing both apo A-I and apo A-II (LPA-I + A-II).
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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.