The DOI matches its Crossref record; 235 of the 238 references it cites were found in a registry or an index.
Metabolism of triglyceride-rich lipoproteins in health and dyslipidaemia
Abstract
Accumulating evidence points to the causal role of triglyceride-rich lipoproteins and their cholesterol-enriched remnants in atherogenesis. Genetic studies in particular have not only revealed a relationship between plasma triglyceride levels and the risk of atherosclerotic cardiovascular disease, but have also identified key proteins responsible for the regulation of triglyceride transport. Kinetic studies in humans using stable isotope tracers have been especially useful in delineating the function of these proteins and revealing the hitherto unappreciated complexity of triglyceride-rich lipoprotein metabolism. Given that triglyceride is an essential energy source for mammals, triglyceride transport is regulated by numerous mechanisms that balance availability with the energy demands of the body. Ongoing investigations are focused on determining the consequences of dysregulation as a result of either dietary imprudence or genetic variation that increases the risk of atherosclerosis and pancreatitis. The identification of molecular control mechanisms involved in triglyceride metabolism has laid the groundwork for a 'precision-medicine' approach to therapy. Novel pharmacological agents under development have specific molecular targets within a regulatory framework, and their deployment heralds a new era in lipid-lowering-mediated prevention of disease. In this Review, we outline what is known about the dysregulation of triglyceride transport in human hypertriglyceridaemia.
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In the citing paper
“A decrease of 1 mmol/L (88.57 mg/dL) in triglycerides has been linked to roughly a 25% reduction in cardiovascular disease risk [24, 25]”
From Ketogenic diet-induced changes in adult lipid metabolism: a comprehensive systematic review and meta-regression of randomized controlled trials (2026) · cites this paper as [24]
In the citing paper
“In the postprandial state, CM are assembled in enterocytes through the packaging of dietary TG, cholesterol, and apolipoprotein B48 [10].”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [10]
In the citing paper
“In parallel, hepatocytes continuously secrete VLDL particles containing apolipoprotein B100, incorporating TG derived from de novo lipogenesis, circulating non-esterified fatty acids, hepatic lipid stores, and remnant uptake [10].”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [10]
In the citing paper
“TRLs, primarily chylomicrons (CM) and very low-density lipoproteins (VLDL), are secreted by the intestine and liver, respectively, and are the main vehicles for TG transport in the circulation.”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [10]
In the citing paper
“Hypercholesterolemia, defined by elevated plasma low‐density lipoprotein (LDL) cholesterol, is a well‐established risk factor not only for cardiovascular disease (Borén et al. 2022; Steinberg 2013; Tabas et al. 2015; Boffa and Koschinsky 2019), but also for cognitive decline and dementia in later life (Kivipelto et al. 2001; Kivipelto and Solomon 2006; Livingston et al. 2024; Sparks et al. 2000, 2”
From LDL Cholesterol Modulates Astrocyte Metabolism, Lipid Handling, and Morphology: Evidence From In Vitro and In Vivo Models (2026) · cites this paper as Borén et al. 2022
Citations
Cites
Mach, F., Baigent, C., Catapano, A. L., Koskinas, K. C., Casula, M., Badimon, L., Chapman, M. J., De Backer, G. G., Delgado, V., Ference, B. A., et al. (2020) · European Heart Journal · doi:10.1093/eurheartj/ehz455 · Cited by 8,961
Self-citationMach, F., Baigent, C., Catapano, A. L., Koskinas, K. C., Casula, M., Badimon, L., Chapman, M. J., De Backer, G. G., Delgado, V., Ference, B. A., et al. (2019) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2019.08.014 · Cited by 4,854
Self-citation(2019) · doi:10.1161/cir.0000000000000677 · Cited by 4,501
Donnelly, K. L., Smith, C. I., Schwarzenberg, S. J., Jessurun, J., Boldt, M. D., & Parks, E. J. (2005) · Journal of Clinical Investigation · doi:10.1172/jci23621 · Cited by 3,604
Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia
Bhatt, D. L., Steg, P. G., Miller, M., Brinton, E. A., Jacobson, T. A., Ketchum, S. B., Doyle, R. T., Juliano, R. A., Jiao, L., Granowitz, C., et al. (2019) · New England Journal of Medicine · doi:10.1056/nejmoa1812792 · Cited by 3,317
Effects of Combination Lipid Therapy in Type 2 Diabetes Mellitus
(2010) · New England Journal of Medicine · doi:10.1056/nejmoa1001282 · Cited by 2,837
Major lipids, apolipoproteins, and risk of vascular disease
The Emerging Risk Factors Collaboration* (2009) · JAMA · doi:10.1001/jama.2009.1619 · Cited by 2,731
Mechanisms and disease consequences of nonalcoholic fatty liver disease
Loomba, R., Friedman, S. L., & Shulman, G. I. (2021) · Cell · doi:10.1016/j.cell.2021.04.015 · Cited by 2,002
Molecular mediators of hepatic steatosis and liver injury
Browning, J. D., & Horton, J. D. (2004) · Journal of Clinical Investigation · doi:10.1172/jci200422422 · Cited by 1,772
Research works printed but not linked: 1
- Chan, L. et al. From editosome to proteasome. Recent. Prog. Horm. Res. 55, 93–125 (2000). discussion 126.
Cited by
Sorted by citations
Björnson, E., Adiels, M., Taskinen, M.-R., Burgess, S., Rawshani, A., Borén, J., & Packard, C. J. (2023) · European Heart Journal · doi:10.1093/eurheartj/ehad337 · Cited by 183
“1–5 In analogy with the pathogenic mechanisms linked to low-density lipoproteins (LDL), remnant lipoproteins can penetrate the sub-endothelial space in artery walls and bind to proteoglycans, thereby initiating cholesterol deposition and foam cell formation.”
Self-citationLi, Z., Zhang, B., Liu, Q., Tao, Z., Ding, L., Guo, B., Zhang, E., Zhang, H., Meng, Z., Guo, S., et al. (2023) · EBioMedicine · doi:10.1016/j.ebiom.2023.104543 · Cited by 136
Zhao, Y., Zhuang, Z., Li, Y., Xiao, W., Song, Z., Huang, N., Wang, W., Dong, X., Jia, J., Clarke, R., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-46686-x · Cited by 117
Xu, H., She, P., Zhao, Z., Ma, B., Li, G., & Wang, Y. (2023) · Advanced Materials · doi:10.1002/adma.202300439 · Cited by 103
Apolipoprotein B-containing lipoproteins in atherogenesis
Borén, J., Packard, C. J., & Binder, C. J. (2025) · Nature Reviews Cardiology · doi:10.1038/s41569-024-01111-0 · Cited by 110
Self-citation
Metadata
- Authors
- Borén, J., Taskinen, M.-R., Björnson, E., & Packard, C. J.
- Affiliations
- University of Gothenburg (SE)
- University of Helsinki (FI)
- University of Glasgow (GB)
- Corresponding author
- Borén, Jan
- Venue
- Nature Reviews Cardiology
- Published
- 2022-03-22
- Volume
- 19
- Issue
- 9
- Pages
- 577-592
- ISSN
- 1759-5002 (ISSN-L)
- 1759-5010
- OpenAlex
- W4220891222
- Semantic Scholar
- 43b00c155f869658a4650440b8527740c6158985
- Cited by
- 315
- References
- 238
- Citations by year
- 2026: 74 · 2025: 99 · 2024: 78 · 2023: 48 · 2022: 14
- FWCI
- 12.34
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature Reviews Cardiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Keywords
- triglyceride-rich lipoproteins, lipoprotein metabolism, hypertriglyceridemia, dyslipidemia, atherogenesis, atherosclerotic cardiovascular disease, triglyceride transport, lipoprotein lipase, hepatic lipase, cholesteryl ester transfer protein, stable isotope tracers, genetic variation, pancreatitis, lipid-lowering therapy, precision medicine
- MeSH terms
- Animals, Humans, Kinetics, Lipoproteins, Mammals, Triglycerides, Hypertriglyceridemia, Dyslipidemias, Atherosclerosis
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