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The Roles of ApoC-III on the Metabolism of Triglyceride-Rich Lipoproteins in Humans
Open accessAbstract
Cardiovascular disease (CVD) is the leading cause of death globally. It is well established based on evidence accrued during the last three decades that high plasma concentrations of cholesterol-rich atherogenic lipoproteins are causatively linked to CVD, and that lowering these reduces atherosclerotic cardiovascular events in humans.1-9 Historically, most attention has been on low-density lipoproteins (LDL) since these are the most abundant atherogenic lipoproteins in the circulation, and thus the main carrier of cholesterol into the artery wall. However, with the rise of obesity and insulin resistance in many populations, there is increasing interest in the role of triglyceride-rich lipoproteins (TRLs) and their metabolic remnants, with accumulating evidence showing they too are causatively linked to CVD. Plasma triglyceride, measured either in the fasting or non-fasting state, is a useful index of the abundance of TRLs and recent research into the biology and genetics of triglyceride heritability has provided new insight into the causal relationship of TRLs with CVD. Of the genetic factors known to influence plasma triglyceride levels variation in APOC3 - the gene for apolipoprotein (apo) C-III - has emerged as being particularly important as a regulator of triglyceride transport and a novel therapeutic target to reduce dyslipidaemia and CVD risk.
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“Moreover, the reduction in apolipoprotein C-III levels by the conventional triglyceride-lowering agents, such as fibrates and omega-3 fatty acids, is modest (10 to 40%)”
From Olezarsen, Acute Pancreatitis, and Familial Chylomicronemia Syndrome (2024) · cites this paper as [34]
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“Elevated apoC-III levels are associated with increased circulating TG, impaired remnant clearance, and a heightened burden of atherogenic lipoproteins.”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [111]
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“beyond its inhibitory action on lipoprotein lipase (LPL), apoC-III also delays hepatic uptake of TRL remnants, contributing to both hypertriglyceridemia and atherosclerotic progression through LPL-independent pathways [111]”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [111]
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“and these agents have not been effective in lowering triglyceride levels in patients with familial chylomicronemia syndrome. 21,34”
From Olezarsen, Acute Pancreatitis, and Familial Chylomicronemia Syndrome (2024) · cites this paper as [34]
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“Residual clearance was delayed in patients with apoE dysfunction [such as type III hyperlipidemia (18)], while apoC-III has been confirmed as an inhibitor of TRL clearance (19).”
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“This APOC3 gene encodes a component of VLDL (apolipoprotein C3) that inhibits lipoprotein and hepatic lipase, and loss of APOC3 protein function was associated with high triglycerides [179].”
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“The enhanced combination may be attributed to conformational changes connected with high Apo CIII content, making Apo B or Apo E more approachable to PGs 64,65 .”
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Self-citationSigala, D. M., Hieronimus, B., Medici, V., Lee, V., Nuñez, M. V., Bremer, A. A., Cox, C. L., Price, C. A., Benyam, Y., Abdelhafez, Y. G., et al. (2022) · Nutrients · doi:10.3390/nu14081648 · Cited by 17
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“…mechanisms, including increased hepatic clearance of TRL, reduced VLDL secretion, and reduced intestinal lipid absorption of dietary TG. 77,78 Two medications in this class are olezarsen (an antisense oligonucleotide targeting apoC-III) and plozasiran (a small interfering RNA [siRNA]…”
Saadatagah, S., Larouche, M., Naderian, M., Nambi, V., Brisson, D., Kullo, I. J., Duell, P. B., Michos, E. D., Shapiro, M. D., Watts, G. F., et al. (2025) · American Journal of Preventive Cardiology · doi:10.1016/j.ajpc.2025.100978 · Cited by 16
“Inhibition or decreased production of apoC-III can dramatically reduce TG through both LPL-dependent and -independent mechanisms, including increased hepatic clearance of TRL, reduced VLDL secretion, and reduced intestinal lipid absorption of dietary TG [77,78].”
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“If ApoC-III is not tightly regulated it can lead to hypertriglyceridemia and an increased risk of cardiovascular disease (Boren et al., 2020).”
BackgroundOlezarsen, a liver-directed APOC3 ASO therapy for hypertriglyceridemia
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“Apolipoprotein (apo)C-III, a glycoprotein found on TRL and their remnants, increases circulating TG levels by several mechanisms, including inhibiting lipoprotein lipase (LPL) and reducing the hepatic clearance of TRL remnants [14,15].”
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Large-Scale Analysis of Apolipoprotein CIII Glycosylation by Ultrahigh Resolution Mass Spectrometry
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Recent Apolipoprotein CIII trials
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“The rational for this is based on the findings that this apoprotein functions as an important regulator of TGs transport [19,20].”
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“However, under normal metabolism, ApoC3 is rarely found in LDL [36].”
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“It has detrimental effects on the vascular wall by reducing the clearance of TRLs via lipoprotein lipase (LPL)-dependent and -independent pathways [7].”
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Sztolsztener, K., Żywno, H., Hodun, K., Konończuk, K., Muszyńska-Rosłan, K. M., & Latoch, E. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms231810634 · Cited by 11
“Increased levels of Apo-C3 and Apo-H induce inhibition of triacylglycerol-rich lipoprotein (TRL) lipolysis and impair the hepatic TRL clearance, which may result in hypertriglyceridemia and the formation of atherosclerotic plaques, thereby significantly increasing the risk of cardiovascular disorders [45,46].”
BackgroundRNA interference-based therapies for the control of atherosclerosis risk factors
Kettunen, S., Ruotsalainen, A., & Ylä‐Herttuala, S. (2022) · Current Opinion in Cardiology · doi:10.1097/hco.0000000000000972 · Cited by 10
A New Modality in Dyslipidemia Treatment: Antisense Oligonucleotide Therapy
Kim, K., & Choi, S. H. (2022) · Journal of Lipid and Atherosclerosis · doi:10.12997/jla.2022.11.3.250 · Cited by 11
Pérez‐Vega, K. A., Castañer, O., Sanllorente, A., Lassale, C. M., Ros, E., Pintó, X., Estruch, R., Salas‐Salvadó, J., Corella, D., Alonso‐Gómez, Á. M., et al. (2022) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.202200338 · Cited by 8
Apolipoprotein-CIII O-Glycosylation, a Link between GALNT2 and Plasma Lipids
Naber, A., Demus, D., Slieker, R. C., Nicolardi, S., Beulens, J. W. J., Elders, P. J. M., Lieverse, A. G., Sijbrands, E. J. G., Hart, L. M. ‘., Wuhrer, M., et al. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241914844 · Cited by 9
Kanter, J. E., & Bornfeldt, K. (2020) · Journal of Lipid Research · doi:10.1194/jlr.ilr120001217 · Cited by 9
“APOC3 plays a critical role in slowing clearance of triglyceride-rich lipoproteins and their remnant lipoprotein particles (4).”
BackgroundSrivastava, R. A. K. (2023) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2023.08.010 · Cited by 8
Genetics of remnant cholesterol
Wulff, A. B., & Nordestgaard, B. G. (2025) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000991 · Cited by 8
Zhou, X., Gu, Y., & Li, L. (2025) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2025.123620 · Cited by 8
Khudyakov, J. I., Holser, R. R., Vierra, C., Ly, S., Niel, T. K., Hasan, B. B., Crocker, D. E., & da Costa, D. P. (2022) · Journal of Experimental Biology · doi:10.1242/jeb.243572 · Cited by 8
Rout, M., Lerner, M. R., Blackett, P. R., Peyton, M. D., Stavrakis, S., Sidorov, E. V., & Sanghera, D. K. (2022) · American Heart Journal Plus Cardiology Research and Practice · doi:10.1016/j.ahjo.2022.100128 · Cited by 8
“3) containing the APOA5-APOA4-APOC3-APOA1 gene cluster to have a robust association with TRLs with strong reproducibility [9-13].”
BackgroundGenetic Markers Predisposing to Nonalcoholic Steatohepatitis
Sohal, A., Chaudhry, H., & Kowdley, K. V. (2023) · Clinics in Liver Disease · doi:10.1016/j.cld.2023.01.006 · Cited by 9
Recio-López, P., Valladolid‐Acebes, I., Berggren, P., & Juntti‐Berggren, L. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms23010062 · Cited by 8
Akram, M. A., Khodja, A., Dalibalta, S., & Majdalawieh, A. F. (2025) · Current Medicinal Chemistry · doi:10.2174/0109298673348217241119063941 · Cited by 8
Yang, X., Alexander, V. J., Xia, S., & Tsimikas, S. (2025) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2025.120462 · Cited by 7
Treating Cardiovascular Disease with Liver Genome Engineering
Hurley, A. E., & Lagor, W. R. (2022) · Current Atherosclerosis Reports · doi:10.1007/s11883-022-00986-z · Cited by 7
Packard, C. J., Taskinen, M., Björnson, E., Matikainen, N., Söderlund, S., Andersson, L. K., Adiels, M., & Borén, J. (2025) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2025.119166 · Cited by 7
Self-citationPotential of Phage Display Antibody Technology for Cardiovascular Disease Immunotherapy
Yeoh, S. G., Sum, J.-S., Lai, J. Y., Isa, W. Y. H. W., & Lim, T. S. (2021) · Journal of Cardiovascular Translational Research · doi:10.1007/s12265-021-10169-x · Cited by 7
Managing of dyslipidaemia characterized by accumulation of triglyceride-rich lipoproteins
Visser, J., van Zwol, W., & Kuivenhoven, J. A. (2022) · Current Atherosclerosis Reports · doi:10.1007/s11883-022-00979-y · Cited by 7
Xu, Y., Guo, J., Zhang, L., Miao, G., Lai, P., Zhang, W., Liu, L., Hou, X., Wang, Y., Huang, W. Y., et al. (2022) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2022.840358 · Cited by 7
“A growing body of evidence demonstrates that increased plasma ApoC3 levels are positively associated with elevated circulating TG concentration and increased incidence of CVD in independent population-based studies (12).”
BackgroundHypertriglyceridemia, a causal risk factor for atherosclerosis, and its laboratory assessment
Wieczorek, E., Ćwiklińska, A., & Jankowski, M. (2022) · Clinical Chemistry and Laboratory Medicine (CCLM) · doi:10.1515/cclm-2022-0189 · Cited by 7
Björnson, E., Packard, C. J., Adiels, M., Leeper, N. J., Hellawell, J. L., Gummesson, A., Nissen, S. E., & Borén, J. (2025) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwaf657 · Cited by 6
Self-citationGenetic Assessment and Clinical Correlates in Severe Hypertriglyceridemia: A Systematic Review
Luca, C. D., Ciciola, P., D’Errico, G., Taranto, M. D. D., Fortunato, G., Gross, C., Garn, J., Iannuzzo, G., Minno, M. N. D. D., & Calcaterra, I. L. (2025) · Genes · doi:10.3390/genes16111377 · Cited by 7
“[20,21].”
Björnson, E., Adiels, M., Taskinen, M., Packard, C. J., & Borén, J. (2026) · Current Atherosclerosis Reports · doi:10.1007/s11883-026-01399-y · Cited by 8
“Apolipoprotein C-III (apoC-III) has emerged as a key regulator of triglyceride metabolism and an important cardiovascular risk factor [1–3].”
Self-citationEmerging agents targeting triglycerides
Prakash, Y. S., Bhatt, D. L., & Malick, W. A. (2025) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000979 · Cited by 7
Treatment of the metabolic syndrome by siRNA targeting apolipoprotein CIII
Recio-López, P., Valladolid‐Acebes, I., Hadwiger, P., Hoßbach, M., Krampert, M., Prata, C. A. H., Berggren, P., & Juntti‐Berggren, L. (2022) · BioFactors · doi:10.1002/biof.1885 · Cited by 6
“There are some evidences, although mostly from in vitro experiments, that it might be more potent than ASO.25–29 Therefore, the aim of this study was to develop siRNAs targeting mouse liver apoCIII and in vivo test the effects in obese, insulin resistant type-2 diabetic ob/ob mouse.”
BackgroundInfluentialChan, D. C., Ying, Q., & Watts, G. F. (2021) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000795 · Cited by 6
“Plasma apoCIII levels are highly associated with plasma triglyceride concentrations [28,29].”
BackgroundCabodevilla, A. G., Izquierdo, M. C., Basu, D., Younis, W., Tirumalasetty, M. B., Miao, Q. R., Nasias, D., Kanter, J. E., Ho, T. W. W., Gjini, J., et al. (2026) · Nature Communications · doi:10.1038/s41467-025-68193-3 · Cited by 5
“In line with this belief, recent studies of potent TG-reducing therapies have suggested an anti-atherogenic bene fi t not because of their reduction of VLDL and postprandial lipemia, but because they reduce remnant lipoproteins 8,9 .”
Unanticipated Enhancement of Intestinal TG Output by Apoc3 ASO Inhibition
Syed‐Abdul, M. M., Tian, L., & Lewis, G. F. (2023) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.123.319765 · Cited by 4
Rehues, P., Girona, J., Guardiola, M., Ozcariz, E., Amigó, N., Rosales, R., Esteban, Y., Banús, H., Alsina, G. G., González-Lleó, A. M., et al. (2024) · Cardiovascular Diabetology · doi:10.1186/s12933-024-02531-5 · Cited by 6
ApoC3 is expressed in oocytes and increased expression is associated with PCOS progression
Zhou, J., Mo, H., Feng, Q., Li, L., & La, J. (2023) · Journal of Ovarian Research · doi:10.1186/s13048-023-01263-6 · Cited by 5
“An increased plasma level of ApoC3 in states associated with insulin resistance [54].”
BackgroundO-glycoprofiling of Serum Apolipoprotein C-III in Colorectal Cancer
Kianičková, K., Pakanová, Z., Květoň, F., Holazová, A., Kundalia, P. H., Baráth, P., Miljuš, G., Nedić, O., & Katrlı́k, J. (2024) · Frontiers in Bioscience-Landmark · doi:10.31083/j.fbl2901032 · Cited by 5
“The transcription rate of apoC-III is decreased by insulin [38,49] and peroxisome proliferator-activated receptor-α (PPAR α ) [50,51].”
BackgroundTakashima, M., Taniguchi, K., Nagaya, M., Yamamura, S., Takamura, Y., Inatani, M., & Oki, M. (2023) · Scientific Reports · doi:10.1038/s41598-023-45088-1 · Cited by 5
“APOC3 is an apolipoprotein, and Apoc3 mutations potentially dysregulate metabolism of lipids and cholesterol, which is likely to contribute to cataract formation 43,45 .”
Background
Metadata
- Authors
- Borén, J., Packard, C. J., & Taskinen, M.-R.
- Affiliations
- University of Gothenburg (SE)
- University of Glasgow (GB)
- University of Helsinki (FI)
- Corresponding author
- Borén, Jan
- Venue
- Frontiers in Endocrinology
- Publisher
- Frontiers Media SA
- Published
- 2020-07-28
- Volume
- 11
- Pages
- 474-474
- ISSN
- 1664-2392 (ISSN-L)
- PMC
- PMC7399058
- OpenAlex
- W3045911834
- Cited by
- 196
- References
- 149
- Citations by year
- 2026: 46 · 2025: 35 · 2024: 30 · 2023: 32 · 2022: 35 · 2021: 17 · 2020: 1
- FWCI
- 3.61
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Endocrinology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Työväentutkimus Vuosikirja (submittedVersion)
- Funders
- Vetenskapsrådet
- Hjärt-Lungfonden
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- apolipoprotein C-III, triglyceride-rich lipoproteins, triglyceride metabolism, cardiovascular disease, dyslipidemia, plasma triglycerides, atherogenic lipoproteins, triglyceride transport, obesity, insulin resistance
- MeSH terms
- Cardiovascular Diseases, Humans, Lipoproteins, Triglycerides, Atherosclerosis, Lipid Metabolism, Apolipoprotein C-III
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