ReviewFrontiers in endocrinology2025
ANGPTL3 and residual atherosclerotic risk: from lipid metabolism to therapeutic targeting.
Review in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Review
- Metabolic disorder-MASLD-cardiovascular disease-kidney disease (MMCK) syndrome: an expansion of the Cardiovascular-Kidney-Metabolic (CKM) framework.Cardiovascular diabetology. Endocrinology reports · 2026Review
- Lipid changes after interleukin-6 blockade in rheumatoid arthritis: beyond cholesterol elevation toward hepatic inflammatory-lipoprotein remodeling.Frontiers in cardiovascular medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite achieving recommended low-density lipoprotein cholesterol (LDL-C) targets, many patients remain at high risk of cardiovascular events due to elevated triglyceride-rich lipoproteins and remnants. Angiopoietin-like protein 3 (ANGPTL3) has emerged as a promising therapeutic target for addressing this residual risk. As a liver-secreted regulator of lipoprotein metabolism, ANGPTL3 influences triglycerides, LDL-C, and high-density lipoprotein cholesterol through inhibition of lipoprotein lipase and endothelial lipase. Human genetic studies and pharmacologic interventions consistently show that ANGPTL3 inhibition improves lipid profiles and lowers apolipoprotein B-containing lipoproteins, independent of LDL receptor function. This review integrates biological, genetic, and clinical evidence, and provides an overview of novel ANGPTL3-targeted therapies, offering new perspectives for cardiovascular prevention and lipid management.
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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.