ReviewJournal of lipid and atherosclerosis2023
New Therapeutic Approaches to the Treatment of Dyslipidemia 1: ApoC-III and ANGPTL3.
Review in Journal of lipid and atherosclerosis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 17 citations in OpenAlex.
- Efficacy of plasma exchange and exchange transfusion in the clinical management of severe hypertriglyceridemia in emergency.Molecular genetics and metabolism reports · 2026Article
- A Layered Framework for Biological Aesthetics: A Narrative Review of Regenerative Medicine in Cosmetic Science.Cureus · 2026Review
- RNA-Targeted Therapeutics for Lipid Metabolic Disorders: From Bench to Bedside.Research (Washington, D.C.) · 2026Article
- Fenofibrate therapy and risk of heart failure outcomes in patients with Type 2 diabetes: a propensity-matched cohort study.European heart journal. Cardiovascular pharmacotherapy · 2025 · on this mapObservational
- Diabetes mediates the association between uric acid to high-density lipoprotein cholesterol ratio and abdominal aortic calcification: a cross-sectional study.Scientific reports · 2025Article
- Time-Restricted Eating, ANGPTL4, and Reduction in Residual Cardiovascular Risk.Journal of clinical medicine · 2025Article
- Dyslipidemia Treatment in Patients with Acute Coronary Syndrome: Is It Time to Move to Combination Therapy?Journal of clinical medicine · 2025Review
- Triglycerides, Triglyceride-Rich Lipoproteins, and Remnant Cholesterol in Atherosclerotic Cardiovascular Disease.Journal of lipid and atherosclerosis · 2025Review
- Angiopoietin-like Proteins and Lipoprotein Lipase: The Waltz Partners That Govern Triglyceride-Rich Lipoprotein Metabolism? Impact on Atherogenesis, Dietary Interventions, and Emerging Therapies.Journal of clinical medicine · 2024Article
- Sugar and Dyslipidemia: A Double-Hit, Perfect Storm.Journal of clinical medicine · 2023Review
- Triglyceride-Rich Lipoprotein Metabolism: Key Regulators of Their Flux.Journal of clinical medicine · 2023Review
- Review
- The chylomicron saga: time to focus on postprandial metabolism.Frontiers in endocrinology · 2023Review
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
Low-density lipoprotein cholesterol (LDL-C)-lowering therapy that increases LDL receptor expression in several ways robustly reduces the risk of atherosclerotic cardiovascular disease (CVD). However, a substantial risk of CVD still remains after intensive LDL-C reduction, which requires new treatment modalities for dyslipidemia and cardiovascular risk management. Triglycerides (TGs) and triglyceride-rich lipoproteins (TRLs) have received attention as indicators of residual cardiovascular risk and as direct causal factors for atherosclerosis and CVDs. Advances in understanding TG and TRL metabolism and their association with clinically evident CVDs have led to the development of novel therapeutic targets, including apolipoprotein C-III (apoC-III) and angiopoietin-like protein 3 (ANGPTL3). Genetic association studies have indicated that both apoC-III and ANGPTL3 play a causal role in the development of atherosclerotic CVD. Both molecules contribute to lipid dysregulation and atherosclerosis primarily by inhibiting lipoprotein lipase; however, recent evidence has shown that novel pathways exist in relation to their lipid-modifying activities. Notably, recent progress in therapeutic approaches, such as monoclonal antibodies or antisense oligonucleotides, has led to several novel therapeutics targeting apoC-III and ANGPTL3. This review summarized the recent updates and discussions related to apoC-III and ANGPTL3 expression.
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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.