Remnant-like particles accelerate endothelial progenitor cells senescence and induce cellular dysfunction via an oxidative mechanism

Liu, Ling; Wen, Tie; Zheng, Xiao‐Yan; Yang, Deguang; Zhao, Shui‐Ping; Xu, Danyan; Li, Guohua

doi:10.1016/j.atherosclerosis.2008.05.024

Cited by 48 publications

(34 citation statements)

References 45 publications

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“…RLPs are a by-product of TRL that can be isolated from the postprandial plasma of hypertriglyceridemic subjects; they are intestinal (ie, CMRs) or liver-derived (eg, VLDL remnants) TRLs that have undergone partial hydrolysis by LPL. Liu et al 64 have shown that these particles can accelerate senescence and interfere with the function of endothelial progenitor cells; these cells play an important role in the organismal reparative response to in vivo vessel wall injury. Postprandial TRL (ppTG) has also been shown to increase the expression of proinflammatory genes (eg, interleukin-6, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and monocyte chemotactic protein-1), 65 induce apoptosis, 66 and accentuate the inflammatory response of cultured endothelial cells to tumor necrosis factor-␣.…”

Section: Remnant Lipoprotein Particlesmentioning

confidence: 99%

Triglycerides and Cardiovascular Disease

Miller¹,

Stone²,

Ballantyne³

et al. 2011

Circulation

1,590

902

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Section: Remnant Lipoprotein Particlesmentioning

confidence: 99%

Triglycerides and Cardiovascular Disease

Miller¹,

Stone²,

Ballantyne³

et al. 2011

Circulation

1,590

902

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“…Glycophosphatidylinositol HDL-binding protein-1 transfers LPL across and tethers it to the endothelial surface, whereas ApoA5 interacts with LPL to promote chylomicron hydrolysis (77). Hydrolysis of chylomicron TGs by LPL yields remnant particles that are potentially atherogenic (11,89). These remnant particles are removed from the circulation by the liver.…”

Section: Chylomicron Clearance From the Circulationmentioning

confidence: 99%

“…These remnant particles, relatively rich in cholesteryl ester, can increase macrophage foam cell formation, a key step in atherosclerosis (11). In addition, remnant particles can alter endothelial function by promoting progenitor cell senescence (89) and apoptosis (138) response to TNF-α (152). FFA generated from TRL lipolysis can also induce endothelial inflammation (161).…”

Section: Chylomicrons and Atherosclerosismentioning

confidence: 99%

New Insights into the Regulation of Chylomicron Production

Dash

Xiao²,

Morgantini³

et al. 2015

Annu. Rev. Nutr.

147

107

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Dietary lipids are efficiently absorbed by the small intestine, incorporated into triglyceride-rich lipoproteins (chylomicrons), and transported in the circulation to various tissues. Intestinal lipid absorption and mobilization and chylomicron synthesis and secretion are highly regulated processes. Elevated chylomicron production rate contributes to the dyslipidemia seen in common metabolic disorders such as insulin-resistant states and type 2 diabetes and likely increases the risk for atherosclerosis seen in these conditions. An in-depth understanding of the regulation of chylomicron production may provide leads for the development of drugs that could be of therapeutic utility in the prevention of dyslipidemia and atherosclerosis. Chylomicron secretion is subject to regulation by various factors, including diet, body weight, genetic variants, hormones, nutraceuticals, medications, and emerging interventions such as bariatric surgical procedures. In this review we discuss the regulation of chylomicron production, mechanisms that underlie chylomicron dysregulation, and potential avenues for future research.

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“…Such residual risk may reflect aspects of atherogenesis not captured by LDL‐C, including effects of very‐low‐density lipoproteins (VLDLs) and their contents (cholesterol and triglycerides) 5, 6, 7, 8, 9. Enzymatic hydrolysis of VLDL results in the formation of smaller, cholesterol‐enriched lipoprotein particles,5, 10, 11 which experimental studies suggest could contribute to the development of ASCVD 5, 7, 10, 12, 13, 14, 15, 16. Clinically, however, there has been uncertainty as to whether ASCVD events could be further reduced by reducing these triglyceride‐rich lipoproteins, with several neutral trials examining this strategy to date 10, 17…”

mentioning

confidence: 99%

Residual Risk of Atherosclerotic Cardiovascular Events in Relation to Reductions in Very‐Low‐Density Lipoproteins

Lawler

Akinkuolie

Harada

et al. 2017

JAHA

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BackgroundIt is uncertain whether pharmacological reductions in very‐low‐density lipoproteins (VLDLs), and their component triglyceride and cholesterol could reduce residual risk of atherosclerotic cardiovascular disease (ASCVD) events among individuals in whom low‐density lipoprotein cholesterol (LDL‐C) has been adequately lowered. We examined whether individuals with greater on‐statin reductions in VLDL‐related measures—beyond reductions in LDL‐C—were at further reduced risk of ASCVD.Methods and ResultsIn 9423 participants in the JUPITER (Justification for the Use of Statins in Prevention) trial (NCT00239681), at baseline and on statin we measured standard lipids, 400‐MHz proton nuclear magnetic resonance spectroscopy‐measured VLDL particle subclasses (small, medium, and large VLDL lipoprotein particle concentration), and total VLDL cholesterol mass. Compared with individuals allocated to placebo, we examined risk of incident ASCVD (N=211) among statin‐allocated participants who achieved minimal (

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Remnant-like particles accelerate endothelial progenitor cells senescence and induce cellular dysfunction via an oxidative mechanism

Cited by 48 publications

References 45 publications

Triglycerides and Cardiovascular Disease

Triglycerides and Cardiovascular Disease

New Insights into the Regulation of Chylomicron Production

Residual Risk of Atherosclerotic Cardiovascular Events in Relation to Reductions in Very‐Low‐Density Lipoproteins

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