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Cited by 73Lipid metabolism and disordersLipoproteins and Cardiovascular HealthDiabetes, Cardiovascular Risks, and Lipoproteins

Triglyceride-rich lipoproteins and cardiovascular diseases

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Xu, Dandan, Xie, Lin, Cheng, Cheng, Xue, Fei, Sun, Chaonan·2024·Frontiers in Endocrinology
DOI 10.3389/fendo.2024.1409653PMC PMC11176465
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Abstract

The global prevalence of cardiovascular diseases (CVD) continues to rise steadily, making it a leading cause of mortality worldwide. Atherosclerosis (AS) serves as a primary driver of these conditions, commencing silently at an early age and culminating in adverse cardiovascular events that severely impact patients’ quality of life or lead to fatality. Dyslipidemia, particularly elevated levels of low-density lipoprotein cholesterol (LDL-C), plays a pivotal role in AS pathogenesis as an independent risk factor. Research indicates that abnormal LDL-C accumulation within arterial walls acts as a crucial trigger for atherosclerotic plaque formation. As the disease progresses, plaque accumulation may rupture or dislodge, resulting in thrombus formation and complete blood supply obstruction, ultimately causing myocardial infarction, cerebral infarction, and other common adverse cardiovascular events. Despite adequate pharmacologic therapy targeting LDL-C reduction, patients with cardiometabolic abnormalities remain at high risk for disease recurrence, highlighting the importance of addressing lipid risk factors beyond LDL-C. Recent attention has focused on the causal relationship between triglycerides, triglyceride-rich lipoproteins (TRLs), and their remnants in AS risk. Genetic, epidemiologic, and clinical studies suggest a causal relationship between TRLs and their remnants and the increased risk of AS, and this dyslipidemia may be an independent risk factor for adverse cardiovascular events. Particularly in patients with obesity, metabolic syndrome, diabetes, and chronic kidney disease, disordered TRLs and its remnants levels significantly increase the risk of atherosclerosis and cardiovascular disease development. Accumulation of over-synthesized TRLs in plasma, impaired function of enzymes involved in TRLs lipolysis, and impaired hepatic clearance of cholesterol-rich TRLs remnants can lead to arterial deposition of TRLs and its remnants, promoting foam cell formation and arterial wall inflammation. Therefore, understanding the pathogenesis of TRLs-induced AS and targeting it therapeutically could slow or impede AS progression, thereby reducing cardiovascular disease morbidity and mortality, particularly coronary atherosclerotic heart disease.

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  • Endothelial-bound LPL catalyzes hydrolysis of triglycerides within TRLs, releasing free fatty acids and monoacylglycerols, which induce endothelial dysfunction and local inflammation, stimulating production of proinflammatory cytokines TNF-α, IL-1β, and IL-6.

    “Endothelial-bound lipoprotein lipase (LPL) catalyzes the hydrolysis of triglycerides within TRLs, releasing free fatty acids and monoacylglycerols. These lipolysis products act as bioactive mediators that induce endothelial dysfunction and local inflammation, stimulating the production of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interle”

    From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [18]

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  • The resulting cytokine milieu promotes endothelial activation and upregulation of adhesion molecules VCAM-1 and ICAM-1, facilitating monocyte recruitment into the arterial wall.

    “The resulting cytokine milieu promotes endothelial activation and upregulation of adhesion molecules, including vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), thereby facilitating monocyte recruitment into the arterial wall [18].”

    From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [18]

    In “TRLs promotes AS by subendothelial accumulation” (Figure 2; page unavailable), the paper says pro-inflammatory TRLs activate the endothelium to express adhesion molecules, leading to monocyte recruitment; the figure identifies VCAM-1 and ICAM-1. It does not say that the resulting cytokine milieu drives that endothelial activation: it attributes the activation directly to TRLs and their remnants. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

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References 97 · Cited by 73

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  1. [1]Cheng C Zhang J Li X Xue F Cao L Meng L. NPRC deletion mitigated atherosclerosis by inhibiting oxidative stress, inflammation and apoptosis in ApoE knockout mice. Signal Transduct Target Ther. (2023) 8: 290. doi: 10.1038/s41392-023-01560-y 37553374 PMC10409771 · DOI
  2. [2]Peverelle MR Baradi A Paleri S Lee YS Sultani R Toukhsati SR. Higher long-term adherence to statins in rural patients at high atherosclerotic risk. J Clin Lipidol. (2019) 13: 163–9. doi: 10.1016/j.jacl.2018.11.004 30594444 · DOI
  3. [3]Herrington W Lacey B Sherliker P Armitage J Lewington S. Epidemiology of atherosclerosis and the potential to reduce the global burden of atherothrombotic disease. Circ Res. (2016) 118: 535–46. doi: 10.1161/CIRCRESAHA.115.307611 26892956 · DOI
  4. [5]Libby P Buring JE Badimon L Hansson GK Deanfield J Bittencourt MS. Atherosclerosis. Nat Rev Dis Primers. (2019) 5: 56. doi: 10.1038/s41572-019-0106-z 31420554 · DOI · Paper page
  5. [6]Di Angelantonio E Sarwar N Perry P Kaptoge S Ray KK Thompson A. Major lipids, apolipoproteins, and risk of vascular disease. Jama. (2009) 302: 1993– 2000. doi: 10.1001/jama.2009.1619 19903920 PMC3284229 · DOI · Paper page
  6. [7]Erqou S Kaptoge S Perry PL Di Angelantonio E Thompson A White IR. Lipoprotein(a) concentration and the risk of coronary heart disease, stroke, and nonvascular mortality. Jama. (2009) 302: 412–23. doi: 10.1001/jama.2009.1063 PMC3272390 19622820 · DOI · Paper page
  7. [11]Chapman MJ Ginsberg HN Amarenco P Andreotti F Borén J Catapano AL. Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management. Eur Heart J. (2011) 32: 1345–61. doi: 10.1016/S1567-5688(11)70033-2 PMC3105250 21531743 · DOI
  8. [12]Tall AR Thomas DG Gonzalez-Cabodevilla AG Goldberg IJ. Addressing dyslipidemic risk beyond LDL-cholesterol. J Clin Invest. (2022) 132(1): e148559. doi: 10.1172/JCI148559 34981790 PMC8718149 · DOI · Paper page
  9. [13]Musunuru K Kathiresan S. Surprises from genetic analyses of lipid risk factors for atherosclerosis. Circ Res. (2016) 118: 579–85. doi: 10.1161/CIRCRESAHA.115.306398 PMC4762058 26892959 · DOI · Paper page
  10. [14]Sarwar N Danesh J Eiriksdottir G Sigurdsson G Wareham N Bingham S. Triglycerides and the risk of coronary heart disease: 10,158 incident cases among 262,525 participants in 29 Western prospective studies. Circulation. (2007) 115: 450–8. doi: 10.1161/CIRCULATIONAHA.106.637793 17190864 · DOI · Paper page
  11. [15]Heeren J Scheja L. Metabolic-associated fatty liver disease and lipoprotein metabolism. Mol Metab. (2021) 50: 101238. doi: 10.1016/j.molmet.2021.101238 33892169 PMC8324684 · DOI
  12. [16]Gugliucci A. The chylomicron saga: time to focus on postprandial metabolism. Front Endocrinol (Lausanne). (2023) 14: 1322869. doi: 10.3389/fendo.2023.1322869 38303975 PMC10830840 · DOI
  13. [17]Zhao Y Liu L Yang S Liu G Pan L Gu C. Mechanisms of atherosclerosis induced by postprandial lipemia. Front Cardiovasc Med. (2021) 8: 636947. doi: 10.3389/fcvm.2021.636947 33996937 PMC8116525 · DOI
  14. [18]Alves-Bezerra M Cohen DE. Triglyceride metabolism in the liver. Compr Physiol. (2017) 8(1): 1– 8. doi: 10.1002/cphy.c170012 29357123 PMC6376873 · DOI
  15. [20]Salinas CAA Chapman MJ. Remnant lipoproteins: are they equal to or more atherogenic than LDL? Curr Opin Lipidol. (2020) 31: 132–9. doi: 10.1097/MOL.0000000000000682 32332433 · DOI · Paper page
  16. [21]Sirwi A Hussain MM. Lipid transfer proteins in the assembly of apoB-containing lipoproteins. J Lipid Res. (2018) 59: 1094–102. doi: 10.1194/jlr.R083451 PMC6027923 29650752 · DOI
  17. [22]Olofsson SO Borèn J. Apolipoprotein B: a clinically important apolipoprotein which assembles atherogenic lipoproteins and promotes the development of atherosclerosis. J Intern Med. (2005) 258: 395– 410. doi: 10.1111/j.1365-2796.2005.01556.x 16238675 · DOI
  18. [23]Davidson NO Shelness GS APOLIPOPROTEIN B. mRNA editing, lipoprotein assembly, and presecretory degradation. Annu Rev Nutr. (2000) 20: 169–93. doi: 10.1146/annurev.nutr.20.1.169 10940331 · DOI
  19. [24]Stillemark-Billton P Beck C Borén J Olofsson SO. Relation of the size and intracellular sorting of apoB to the formation of VLDL 1 and VLDL 2. J Lipid Res. (2005) 46: 104–14. doi: 10.1194/jlr.M400296-JLR200 15520448 · DOI
  20. [25]Xiao C Stahel P Lewis GF. Regulation of chylomicron secretion: focus on post-assembly mechanisms. Cell Mol Gastroenterol Hepatol. (2019) 7: 487– 501. doi: 10.1016/j.jcmgh.2018.10.015 30819663 PMC6396431 · DOI
  21. [26]Kawano Y Cohen DE. Mechanisms of hepatic triglyceride accumulation in non-alcoholic fatty liver disease. J Gastroenterol. (2013) 48: 434–41. doi: 10.1007/s00535-013-0758-5 PMC3633701 23397118 · DOI
  22. [27]Ipsen DH Lykkesfeldt J Tveden-Nyborg P. Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease. Cell Mol Life Sci. (2018) 75: 3313–27. doi: 10.1007/s00018-018-2860-6 PMC6105174 29936596 · DOI · Paper page
  23. [28]Gugliucci A. Triglyceride-rich lipoprotein metabolism: key regulators of their flux. J Clin Med. (2023) 12(13): 4399. doi: 10.3390/jcm12134399 37445434 PMC10342861 · DOI
  24. [29]Wang H Eckel RH. Lipoprotein lipase: from gene to obesity. Am J Physiol Endocrinol Metab. (2009) 297: E271–88. doi: 10.1152/ajpendo.90920.2008 19318514 · DOI
  25. [30]Xiao C Hsieh J Adeli K Lewis GF. Gut-liver interaction in triglyceride-rich lipoprotein metabolism. Am J Physiol Endocrinol Metab. (2011) 301: E429–46. doi: 10.1152/ajpendo.00178.2011 21693689 · DOI
  26. [31]Dallinga-Thie GM Franssen R Mooij HL Visser ME Hassing HC Peelman F. The metabolism of triglyceride-rich lipoproteins revisited: new players, new insight. Atherosclerosis. (2010) 211: 1– 8. doi: 10.1016/j.atherosclerosis.2009.12.027 20117784 PMC3924774 · DOI
  27. [33]Duran EK Pradhan AD. Triglyceride-rich lipoprotein remnants and cardiovascular disease. Clin Chem. (2021) 67: 183–96. doi: 10.1093/clinchem/hvaa296 33409533 · DOI
  28. [35]Ginsberg HN Packard CJ Chapman MJ Borén J Aguilar-Salinas CA Averna M. Triglyceride-rich lipoproteins and their remnants: metabolic insights, role in atherosclerotic cardiovascular disease, and emerging therapeutic strategies-a consensus statement from the European Atherosclerosis Society. Eur Heart J. (2021) 42: 4791–806. doi: 10.1093/eurheartj/ehab551 PMC8670783 34472586 · DOI · Paper page
  29. [36]Rosenson RS Shott S Lu L Tangney CC. Hypertriglyceridemia and other factors associated with plasma viscosity. Am J Med. (2001) 110: 488–92. doi: 10.1016/S0002-9343(01)00643-X 11331062 · DOI
  30. [38]Nordestgaard BG. Triglyceride-rich lipoproteins and atherosclerotic cardiovascular disease: new insights from epidemiology, genetics, and biology. Circ Res. (2016) 118: 547–63. doi: 10.1161/CIRCRESAHA.115.306249 26892957 · DOI · Paper page
  31. [39]Packard CJ Remnants LDL. and the quantification of lipoprotein-associated risk in atherosclerotic cardiovascular disease. Curr Atheroscler Rep. (2022) 24: 133–42. doi: 10.1007/s11883-022-00994-z PMC8983627 35175548 · DOI
  32. [40]Raja V Aguiar C Alsayed N Chibber YS ElBadawi H Ezhov M. Non-HDL-cholesterol in dyslipidemia: Review of the state-of-the-art literature and outlook. Atherosclerosis. (2023) 383: 117312. doi: 10.1016/j.atherosclerosis.2023.117312 37826864 · DOI
  33. [41]Wilkins JT Gidding SS Robinson JG. Can atherosclerosis be cured? Curr Opin Lipidol. (2019) 30: 477–84. doi: 10.1097/MOL.0000000000000644 PMC7375463 31592794 · DOI
  34. [42]Li Y Luo X Hua Z Xue X Wang X Pang M. Apolipoproteins as potential communicators play an essential role in the pathogenesis and treatment of early atherosclerosis. Int J Biol Sci. (2023) 19: 4493–510. doi: 10.7150/ijbs.86475 PMC10535700 37781031 · DOI
  35. [43]Borén J Chapman MJ Krauss RM Packard CJ Bentzon JF Binder CJ. Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J. (2020) 41: 2313–30. doi: 10.1093/eurheartj/ehz962 PMC7308544 32052833 · DOI · Paper page
  36. [44]Jackson KG Poppitt SD Minihane AM. Postprandial lipemia and cardiovascular disease risk: Interrelationships between dietary, physiological and genetic determinants. Atherosclerosis. (2012) 220: 22– 33. doi: 10.1016/j.atherosclerosis.2011.08.012 21955695 · DOI · Paper page
  37. [45]Norata GD Grigore L Raselli S Seccomandi PM Hamsten A Maggi FM. Triglyceride-rich lipoproteins from hypertriglyceridemic subjects induce a pro-inflammatory response in the endothelium: Molecular mechanisms and gene expression studies. J Mol Cell Cardiol. (2006) 40: 484–94. doi: 10.1016/j.yjmcc.2006.01.022 16516917 · DOI
  38. [46]Botham KM Wheeler-Jones CP. Postprandial lipoproteins and the molecular regulation of vascular homeostasis. Prog Lipid Res. (2013) 52: 446–64. doi: 10.1016/j.plipres.2013.06.001 23774609 · DOI
  39. [47]Liu L Wen T Zheng XY Yang DG Zhao SP Xu DY. Remnant-like particles accelerate endothelial progenitor cells senescence and induce cellular dysfunction via an oxidative mechanism. Atherosclerosis. (2009) 202: 405–14. doi: 10.1016/j.atherosclerosis.2008.05.024 18582890 · DOI
  40. [48]Koelwyn GJ Corr EM Erbay E Moore KJ. Regulation of macrophage immunometabolism in atherosclerosis. Nat Immunol. (2018) 19: 526–37. doi: 10.1038/s41590-018-0113-3 PMC6314674 29777212 · DOI
  41. [49]Moore KJ Sheedy FJ Fisher EA. Macrophages in atherosclerosis: a dynamic balance. Nat Rev Immunol. (2013) 13: 709–21. doi: 10.1038/nri3520 PMC4357520 23995626 · DOI · Paper page
  42. [50]Tabas I. Macrophage death and defective inflammation resolution in atherosclerosis. Nat Rev Immunol. (2010) 10: 36– 46. doi: 10.1038/nri2675 19960040 PMC2854623 · DOI · Paper page
  43. [51]Virmani R Burke AP Kolodgie FD Farb A. Vulnerable plaque: the pathology of unstable coronary lesions. J Interv Cardiol. (2002) 15: 439–46. doi: 10.1111/j.1540-8183.2002.tb01087.x 12476646 · DOI
  44. [52]Bermúdez B López S Pacheco YM Villar J Muriana FJ Hoheisel JD. Influence of postprandial triglyceride-rich lipoproteins on lipid-mediated gene expression in smooth muscle cells of the human coronary artery. Cardiovasc Res. (2008) 79: 294– 303. doi: 10.1093/cvr/cvn082 18359786 · DOI
  45. [53]Ackers-Johnson M Talasila A Sage AP Long X Bot I Morrell NW. Myocardin regulates vascular smooth muscle cell inflammatory activation and disease. Arterioscler Thromb Vasc Biol. (2015) 35: 817–28. doi: 10.1161/ATVBAHA.114.305218 PMC4390125 25614278 · DOI
  46. [54]Reape TJ Groot PH. Chemokines and atherosclerosis. Atherosclerosis. (1999) 147: 213–25. doi: 10.1016/S0021-9150(99)00346-9 10559506 · DOI
  47. [55]Domoto K Taniguchi T Takaishi H Takahashi T Fujioka Y Takahashi A. Chylomicron remnants induce monocyte chemoattractant protein-1 expression via p38 MAPK activation in vascular smooth muscle cells. Atherosclerosis. (2003) 171: 193– 200. doi: 10.1016/j.atherosclerosis.2003.08.016 14644387 · DOI
  48. [56]Borén J Williams KJ. The central role of arterial retention of cholesterol-rich apolipoprotein-B-containing lipoproteins in the pathogenesis of atherosclerosis: a triumph of simplicity. Curr Opin Lipidol. (2016) 27: 473–83. doi: 10.1097/MOL.0000000000000330 27472409 · DOI · Paper page
  49. [57]Wang Y McNutt MC Banfi S Levin MG Holland WL Gusarova V. Hepatic ANGPTL3 regulates adipose tissue energy homeostasis. Proc Natl Acad Sci U.S.A. (2015) 112: 11630–5. doi: 10.1073/pnas.1515374112 PMC4577179 26305978 · DOI
  50. [58]Shimizugawa T Ono M Shimamura M Yoshida K Ando Y Koishi R. ANGPTL3 decreases very low density lipoprotein triglyceride clearance by inhibition of lipoprotein lipase. J Biol Chem. (2002) 277: 33742–8. doi: 10.1074/jbc.M203215200 12097324 · DOI
  51. [59]Robciuc MR Maranghi M Lahikainen A Rader D Bensadoun A Öörni K. Angptl3 deficiency is associated with increased insulin sensitivity, lipoprotein lipase activity, and decreased serum free fatty acids. Arterioscler Thromb Vasc Biol. (2013) 33: 1706–13. doi: 10.1161/ATVBAHA.113.301397 23661675 · DOI
  52. [61]Sylvers-Davie KL Davies BSJ. Regulation of lipoprotein metabolism by ANGPTL3, ANGPTL4, and ANGPTL8. Am J Physiol Endocrinol Metab. (2021) 321: E493– e508. doi: 10.1152/ajpendo.00195.2021 34338039 PMC8560382 · DOI
  53. [62]Luo F Das A Khetarpal SA Fang Z Zelniker TA Rosenson RS. ANGPTL3 inhibition, dyslipidemia, and cardiovascular diseases. Trends Cardiovasc Med. (2023) 34(4): 215–22. doi: 10.1016/j.tcm.2023.01.008 36746257 · DOI
  54. [63]Mohamed F Mansfield BS Raal FJ. ANGPTL3 as a drug target in hyperlipidemia and atherosclerosis. Curr Atheroscler Rep. (2022) 24: 959–67. doi: 10.1007/s11883-022-01071-1 PMC9650658 36367663 · DOI
  55. [64]Chen PY Gao WY Liou JW Lin CY Wu MJ Yen JH. Angiopoietin-like protein 3 (ANGPTL3) modulates lipoprotein metabolism and dyslipidemia. Int J Mol Sci. (2021) 22(14): 7310. doi: 10.3390/ijms22147310 34298929 PMC8304944 · DOI
  56. [65]Rosenson RS Shaik A Song W. New therapies for lowering triglyceride-rich lipoproteins: JACC focus seminar 3/4. J Am Coll Cardiol. (2021) 78: 1817–30. doi: 10.1016/j.jacc.2021.08.051 PMC9327673 34711341 · DOI
  57. [66]Lupo MG Ferri N. Angiopoietin-like 3 (ANGPTL3) and atherosclerosis: lipid and non-lipid related effects. J Cardiovasc Dev Dis. (2018) 5(3): 39. doi: 10.3390/jcdd5030039 30011918 PMC6162638 · DOI
  58. [67]Gusarova V Alexa CA Wang Y Rafique A Kim JH Buckler D. ANGPTL3 blockade with a human monoclonal antibody reduces plasma lipids in dyslipidemic mice and monkeys. J Lipid Res. (2015) 56: 1308–17. doi: 10.1194/jlr.M054890 PMC4479335 25964512 · DOI · Paper page
  59. [68]Dewey FE Gusarova V Dunbar RL O'Dushlaine C Schurmann C Gottesman O. Genetic and pharmacologic inactivation of ANGPTL3 and cardiovascular disease. N Engl J Med. (2017) 377: 211–21. doi: 10.1056/NEJMoa1612790 PMC5800308 28538136 · DOI · Paper page
  60. [69]Reeskamp LF Nurmohamed NS Bom MJ Planken RN Driessen RS van Diemen PA. Marked plaque regression in homozygous familial hypercholesterolemia. Atherosclerosis. (2021) 327: 13–7. doi: 10.1016/j.atherosclerosis.2021.04.014 34004483 · DOI
  61. [70]Ward NC Chan DC Watts GF. A tale of two new targets for hypertriglyceridaemia: which choice of therapy? BioDrugs. (2022) 36: 121–35. doi: 10.1007/s40259-022-00520-2 PMC8986672 35286660 · DOI
  62. [71]Malick WA Waksman O Do R Koenig W Pradhan AD Stroes ESG. Clinical trial design for triglyceride-rich lipoprotein-lowering therapies: JACC focus seminar 3/3. J Am Coll Cardiol. (2023) 81: 1646–58. doi: 10.1016/j.jacc.2023.02.034 37076219 · DOI
  63. [73]Watts GF Schwabe C Scott R Gladding PA Sullivan D Baker J. RNA interference targeting ANGPTL3 for triglyceride and cholesterol lowering: phase 1 basket trial cohorts. Nat Med. (2023) 29: 2216–23. doi: 10.1038/s41591-023-02494-2 PMC10504078 37626170 · DOI · Paper page
  64. [74]Alexander VJ Xia S Hurh E Hughes SG O'Dea L Geary RS. N-acetyl galactosamine-conjugated antisense drug to APOC3 mRNA, triglycerides and atherogenic lipoprotein levels. Eur Heart J. (2019) 40: 2785–96. doi: 10.1093/eurheartj/ehz209 PMC6736334 31329855 · DOI · Paper page
  65. [75]Gouni-Berthold I Schwarz J Berthold HK. Updates in drug treatment of severe hypertriglyceridemia. Curr Atheroscler Rep. (2023) 25: 701–9. doi: 10.1007/s11883-023-01140-z PMC10564803 37642858 · DOI · Paper page
  66. [76]Jang AY Lim S Jo SH Han SH Koh KK. New trends in dyslipidemia treatment. Circ J. (2021) 85: 759–68. doi: 10.1253/circj.CJ-20-1037 33177309 · DOI
  67. [77]Wang X Musunuru K. Angiopoietin-like 3: from discovery to therapeutic gene editing. JACC Basic Transl Sci. (2019) 4: 755–62. doi: 10.1016/j.jacbts.2019.05.008 PMC6834959 31709322 · DOI
  68. [78]Chadwick AC Evitt NH Lv W Musunuru K. Reduced blood lipid levels with in vivo CRISPR-Cas9 base editing of ANGPTL3. Circulation. (2018) 137: 975–7. doi: 10.1161/CIRCULATIONAHA.117.031335 PMC5830171 29483174 · DOI
  69. [79]Rhee JW Wu JC. Dyslipidaemia: In vivo genome editing of ANGPTL3: a therapy for atherosclerosis? Nat Rev Cardiol. (2018) 15: 259–60. doi: 10.1038/nrcardio.2018.38 PMC6432938 29618844 · DOI
  70. [80]Wu SA Kersten S Qi L. Lipoprotein lipase and its regulators: an unfolding story. Trends Endocrinol Metab. (2021) 32: 48– 61. doi: 10.1016/j.tem.2020.11.005 33277156 PMC8627828 · DOI · Paper page
  71. [81]Clee SM Bissada N Miao F Miao L Marais AD Henderson HE. Plasma and vessel wall lipoprotein lipase have different roles in atherosclerosis. J Lipid Res. (2000) 41: 521–31. doi: 10.1016/S0022-2275(20)32399-3 10744772 · DOI · Paper page
  72. [82]Chistiakov DA Melnichenko AA Myasoedova VA Grechko AV Orekhov AN. Mechanisms of foam cell formation in atherosclerosis. J Mol Med (Berl). (2017) 95: 1153–65. doi: 10.1007/s00109-017-1575-8 28785870 · DOI
  73. [83]Babaev VR Fazio S Gleaves LA Carter KJ Semenkovich CF Linton MF. Macrophage lipoprotein lipase promotes foam cell formation and atherosclerosis in vivo. J Clin Invest. (1999) 103: 1697–705. doi: 10.1172/JCI6117 PMC408384 10377176 · DOI
  74. [84]Generoso G Janovsky C Bittencourt MS. Triglycerides and triglyceride-rich lipoproteins in the development and progression of atherosclerosis. Curr Opin Endocrinol Diabetes Obes. (2019) 26: 109–16. doi: 10.1097/MED.0000000000000468 30694827 · DOI
  75. [85]Li Y He PP Zhang DW Zheng XL Cayabyab FS Yin WD. Lipoprotein lipase: from gene to atherosclerosis. Atherosclerosis. (2014) 237: 597– 608. doi: 10.1016/j.atherosclerosis.2014.10.016 25463094 · DOI
  76. [86]Laufs U Parhofer KG Ginsberg HN Hegele RA. Clinical review on triglycerides. Eur Heart J. (2020) 41: 99– 109c. doi: 10.1093/eurheartj/ehz785 31764986 PMC6938588 · DOI · Paper page
  77. [87]Wieczorek E Ćwiklińska A Jankowski M. Hypertriglyceridemia, a causal risk factor for atherosclerosis, and its laboratory assessment. Clin Chem Lab Med. (2022) 60: 1145–59. doi: 10.1515/cclm-2022-0189 35687325 · DOI
  78. [88]Drexel H Tamargo J Kaski JC Lewis BS Saely CH Fraunberger P. Triglycerides revisited: is hypertriglyceridaemia a necessary therapeutic target in cardiovascular disease? Eur Heart J Cardiovasc Pharmacother. (2023) 9: 570–82. doi: 10.1093/ehjcvp/pvad044 37328424 · DOI
  79. [89]Keech A Simes RJ Barter P Best J Scott R Taskinen MR. Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial. Lancet. (2005) 366: 1849–61. doi: 10.1016/S0140-6736(05)67667-2 16310551 · DOI · Paper page
  80. [90]Bezafibrate Infarction Prevention (BIP) study. Secondary prevention by raising HDL cholesterol and reducing triglycerides in patients with coronary artery disease. Circulation. (2000) 102: 21–7. doi: 10.1161/01.CIR.102.1.21 10880410 · DOI · Paper page
  81. [93]Hegele RA Ginsberg HN Chapman MJ Nordestgaard BG Kuivenhoven JA Averna M. The polygenic nature of hypertriglyceridaemia: implications for definition, diagnosis, and management. Lancet Diabetes Endocrinol. (2014) 2: 655–66. doi: 10.1016/S2213-8587(13)70191-8 PMC4201123 24731657 · DOI · Paper page
  82. [95]Nishizaki Y Miyauchi K Iwata H Inoue T Hirayama A Kimura K. Study protocol and baseline characteristics of Randomized trial for Evaluation in Secondary Prevention Efficacy of Combination Therapy-Statin and Eicosapentaenoic Acid: RESPECT-EPA, the combination of a randomized control trial and an observational biomarker study. Am Heart J. (2023) 257: 1– 8. doi: 10.1016/j.ahj.2022.11.008 36372250 · DOI · Paper page
  83. [96]Sherratt SCR Mason RP Libby P Steg PG Bhatt DL. Do patients benefit from omega-3 fatty acids? Cardiovasc Res. (2024) 119: 2884–901. doi: 10.1093/cvr/cvad188 PMC10874279 38252923 · DOI

Authors
Xu, D., Xie, L., Cheng, C., Xue, F., & Sun, C.
Affiliations
  • Shandong University (CN)
  • Sheng Jing Hospital (CN)
  • Liaoning Cancer Hospital & Institute (CN)
Corresponding author
  • Xue, Fei
  • Sun, Chaonan
ORCID
Venue
Frontiers in Endocrinology
Publisher
Frontiers Media SA
Published
2024-05-31
Volume
15
Pages
1409653-1409653
ISSN
1664-2392 (ISSN-L)
DOI
10.3389/fendo.2024.1409653
PMC
PMC11176465
OpenAlex
W4399246817
Cited by
73
References
97
Citations by year
2026: 43 · 2025: 27 · 2024: 3
FWCI
5.79
Type
journal article
Language
en
Open access
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)
Funders
China Postdoctoral Science Foundation (2023M742124)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
Keywords
triglyceride-rich lipoproteins, atherosclerosis, cardiovascular disease, dyslipidemia, LDL cholesterol, cardiovascular risk factors, foam cell formation, arterial inflammation, coronary artery disease, cardiometabolic risk, obesity, metabolic syndrome, diabetes mellitus, chronic kidney disease, lipolysis
MeSH terms
Animals, Cardiovascular Diseases, Humans, Lipoproteins, Risk Factors, Triglycerides, Dyslipidemias, Atherosclerosis

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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