ReviewJournal of lipid research2024
APOA5 deficiency causes hypertriglyceridemia by reducing amounts of lipoprotein lipase in capillaries.
Review in Journal of lipid research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Decreases in circulating ANGPTL3/8 concentrations following retatrutide treatment parallel reductions in serum lipids.Diabetes, obesity & metabolism · 2025Trial
- Targeting the angiopoietin-like protein 3/8 complex with a monoclonal antibody in patients with mixed hyperlipidemia: a phase 1 trial.Nature medicine · 2025Trial
- Cardiac Lipid Metabolism: Cells, Metabolites, and Rhythms.Circulation research · 2026Review
- Integrative analyses elucidate transcriptional regulatory functions of risk alleles for metabolic liver disease.Nature genetics · 2026Article
- Article
- Effects of fenofibrate on angiopoietin-like 3/4/8 proteins and apolipoprotein A5.Journal of lipid research · 2026Article
- Unveiling novel drug targets for atherosclerosis: A Mendelian randomization analysis.Medicine · 2026Article
- Current and Emerging Pharmacological Therapies for Hypertriglyceridemia.International journal of molecular sciences · 2026Review
- A neutralizing APOA5 monoclonal antibody reduces amounts of lipoprotein lipase in capillaries and triggers hypertriglyceridemia.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Molecular characterization of a rare heterozygousFrontiers in genetics · 2026Article
- Reversibly reduced lipoprotein lipase in APOA5 c.553G>T-related hypertriglyceridemia successfully treated with pemafibrate.Endocrinology, diabetes & metabolism case reports · 2026Article
- Integrative functional genomics reveals transcriptional regulatory function of risk alleles for metabolic liver disease.Research square · 2025Article
- Apolipoprotein A (ApoA) in Neurological Disorders: Connections and Insights.International journal of molecular sciences · 2025Review
- ANGPTL3 and residual atherosclerotic risk: from lipid metabolism to therapeutic targeting.Frontiers in endocrinology · 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
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Apolipoprotein AV (APOA5) deficiency causes hypertriglyceridemia in mice and humans. For years, the cause remained a mystery, but the mechanisms have now come into focus. Here, we review progress in defining APOA5's function in plasma triglyceride metabolism. Biochemical studies revealed that APOA5 binds to the angiopoietin-like protein 3/8 complex (ANGPTL3/8) and suppresses its ability to inhibit the activity of lipoprotein lipase (LPL). Thus, APOA5 deficiency is accompanied by increased ANGPTL3/8 activity and lower levels of LPL activity. APOA5 deficiency also reduces amounts of LPL in capillaries of oxidative tissues (e.g., heart, brown adipose tissue). Cell culture experiments revealed the likely explanation: ANGPTL3/8 detaches LPL from its binding sites on the surface of cells, and that effect is blocked by APOA5. Both the low intracapillary LPL levels and the high plasma triglyceride levels in Apoa5
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