ReviewCurrent atherosclerosis reports2019
Emerging Evidence that ApoC-III Inhibitors Provide Novel Options to Reduce the Residual CVD.
Review in Current atherosclerosis reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- Moderate alcohol consumption and lipoprotein subfractions: a systematic review of intervention and observational studies.Nutrition reviews · 2022Pooled it
- Lipid Challenge Reveals Amplified Apolipoprotein Responses with Preserved Temporal Pattern in Polyendocrine Metabolic Ovarian Syndrome: An Exploratory Study.International journal of molecular sciences · 2026Trial
- Evinacumab in severe hypertriglyceridemia with or without lipoprotein lipase pathway mutations: a phase 2 randomized trial.Nature medicine · 2023Trial
- Postprandial metabolism of apolipoproteins B48, B100, C-III, and E in humans with APOC3 loss-of-function mutations.JCI insight · 2022Trial
- Apolipoprotein C-III reduction in subjects with moderate hypertriglyceridaemia and at high cardiovascular risk.European heart journal · 2022Trial
- The dual glucose-dependent insulinotropic peptide and glucagon-like peptide-1 receptor agonist, tirzepatide, improves lipoprotein biomarkers associated with insulin resistance and cardiovascular risk in patients with type 2 diabetes.Diabetes, obesity & metabolism · 2020Trial
- Hypertriglyceridaemia-Associated Acute Pancreatitis: Pathophysiological Insights and Advances in Clinical Management.Biomedicines · 2026Review
- Review
- Tirzepatide as a multi-organ integrator in metabolic diseases: a review of molecular mechanisms and clinical translation.Endocrine · 2026Review
- APOC3 Promotes DGAT2-Dependent Triglyceride Accumulation in Hepatocytes During Early Metabolic Dysfunction.Biomolecules · 2026Article
- RNA-Targeted Therapeutics for Lipid Metabolic Disorders: From Bench to Bedside.Research (Washington, D.C.) · 2026Article
- Dyslipidemia in Diabetes: Navigating a Complex Landscape for Improved Cardiovascular Outcomes.Clinical medicine insights. Endocrinology and diabetes · 2026Review
- Olezarsen for the Treatment of Hypertriglyceridemia.Methods in molecular biology (Clifton, N.J.) · 2026Review
- Triglyceride-lowering therapies for hepatic steatosis: mechanisms, efficacy, and clinical perspectives.Frontiers in pharmacology · 2026Review
- HDL-Cholesterol and Triglycerides Dynamics: Essential Players in Metabolic Syndrome.Antioxidants (Basel, Switzerland) · 2025Review
- Review
- Efficacy and Safety of Olezarsen in Dyslipidemia: A Systematic Review and Dose-response Meta-analysis of Randomized Controlled Trials.Journal of the Saudi Heart Association · 2025Review
- The Effects of Tirzepatide on Lipid Profile: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.Journal of obesity & metabolic syndrome · 2024Article
- Assessment of ability of AlphaMissense to identify variants affecting susceptibility to common disease.European journal of human genetics : EJHG · 2024Article
- Review
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 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewApolipoprotein C-III (apoC-III) is known to inhibit lipoprotein lipase (LPL) and function as an important regulator of triglyceride metabolism. In addition, apoC-III has also more recently been identified as an important risk factor for cardiovascular disease. This review summarizes the mechanisms by which apoC-III induces hypertriglyceridemia and promotes atherogenesis, as well as the findings from recent clinical trials using novel strategies for lowering apoC-III. RECENT
findingsGenetic studies have identified subjects with heterozygote loss-of-function (LOF) mutations in APOC3, the gene coding for apoC-III. Clinical characterization of these individuals shows that the LOF variants associate with a low-risk lipoprotein profile, in particular reduced plasma triglycerides. Recent results also show that complete deficiency of apoC-III is not a lethal mutation and is associated with very rapid lipolysis of plasma triglyceride-rich lipoproteins (TRL). Ongoing trials based on emerging gene-silencing technologies show that intervention markedly lowers apoC-III levels and, consequently, plasma triglyceride. Unexpectedly, the evidence points to apoC-III not only inhibiting LPL activity but also suppressing removal of TRLs by LPL-independent pathways. Available data clearly show that apoC-III is an important cardiovascular risk factor and that lifelong deficiency of apoC-III is cardioprotective. Novel therapies have been developed, and results from recent clinical trials indicate that effective reduction of plasma triglycerides by inhibition of apoC-III might be a promising strategy in management of severe hypertriglyceridemia and, more generally, a novel approach to CHD prevention in those with elevated plasma triglyceride.
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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.