Long-chain omega-3 fatty acids, fibrates and niacin as therapeutic options in the treatment of hypertriglyceridemia: A review of the literature

Ito, Matthew K.

doi:10.1016/j.atherosclerosis.2015.06.012

Cited by 55 publications

(31 citation statements)

References 96 publications

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“…If not treated promptly, atherosclerosis can cause the ischemia and necrosis of limbs, and eventually result in amputation. Current therapies prevent vein graft atherosclerosis and are essentially limited to lipid-lowering drugs, typically statins [1], fibrates [2], niacin [3], and ezetimibe [4]. Lipid-lowering drugs decrease low-density lipoprotein cholesterol (LDL-C) level and reduce the risk of atherosclerotic cardiovascular diseases.…”

Section: Introductionmentioning

confidence: 99%

Silence of lncRNA UCA1 Represses the Growth and Tube Formation of Human Microvascular Endothelial Cells Through miR-195

Yin

Sun

2018

Cell Physiol Biochem

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Background/Aims: Recent studies have suggested that several lncRNAs contribute to the angiogenic function of endothelial cells. Herein, we set out to reveal whether lncRNA UCA1 has functions in endothelial angiogenesis. Methods: The expression levels of lncRNA UCA1, miR-195 and CCND1 in human microvascular endothelial HMEC-1 cells were altered by transfection. Subsequently, cell viability, migration, tube formation and apoptosis of HMEC-1 cells were respectively assessed. The cross-talk between lncRNA UCA1, miR-195, CCND1, and MEK/ERK and mTOR signaling pathways were investigated by performing qRT-PCR and Western blotting. Results: Silence of lncRNA UCA1 repressed HMEC-1 cells viability, migration, tube formation, and induced apoptosis. Meanwhile, silence of lncRNA UCA1 significantly up-regulated miR-195 expression. These alterations induced by lncRNA UCA1 were further enhanced by miR-195 overexpression, while were attenuated by miR-195 suppression. Moreover, silence of lncRNA UCA1 deactivated MEK/ERK and mTOR signaling pathways via a miR-195-dependent regulation. And the deactivation of MEK/ERK and mTOR signaling pathways led to a down-regulation of CCND1. Conclusion: This study demonstrates that silence of lncRNA UCA1 largely represses microvascular endothelial cells growth and tube formation. Silence of lncRNA UCA1 exerts its function possibly via up-regulation of miR-195, which in turn inactivates MEK/ERK and mTOR signaling pathways, and ultimately represses CCND1 expression.

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Section: Introductionmentioning

confidence: 99%

Silence of lncRNA UCA1 Represses the Growth and Tube Formation of Human Microvascular Endothelial Cells Through miR-195

Yin

Sun

2018

Cell Physiol Biochem

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“…Niacin causes flushing, which many patients find intolerable, and also has the potential to increase serum glucose and cause liver toxicity or myopathy, particularly when coadministered with a statin. 47 Fibrates may blunt the beneficial effects of statins on LDL-C, particularly in patients with atherogenic dyslipidemia, 48 and like niacin, has the potential to cause myopathy when used in combination with a statin. 47 The use of niacin or fibrates in combination with a statin has recently been removed from the labels of several products because of the lack of data showing CV benefit with these combinations.…”

Section: Overview Of Trl Metabolismmentioning

confidence: 99%

Triglycerides and Triglyceride-Rich Lipoproteins in the Causal Pathway of Cardiovascular Disease

Budoff

2016

The American Journal of Cardiology

151

103

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Epidemiologic and clinical studies suggest that elevated triglyceride levels are a biomarker of cardiovascular (CV) risk. Consistent with these findings, recent genetic evidence from mutational analyses, genome-wide association studies, and Mendelian randomization studies provide robust evidence that triglycerides and triglyceride-rich lipoproteins are in the causal pathway for atherosclerotic CV disease, indicating that they may play a pathogenic role, much like low-density lipoprotein cholesterol (LDL-C). Although statins are the cornerstone of dyslipidemia management, high triglyceride levels may persist in some patients despite statin therapy. Several triglyceride-lowering agents are available, including fibrates, niacin, and omega-3 fatty acids, of which prescription omega-3 fatty acids have the best tolerability and safety profile. In clinical studies, omega-3 fatty acids have been shown to reduce triglyceride levels, but products containing both eicosapentaenoic acid and docosahexaenoic acid may increase LDL-C levels. Icosapent ethyl, a high-purity eicosapentaenoic acid-only product, does not raise LDL-C levels and also reduces triglyceride, non-high-density lipoprotein cholesterol, and triglyceride-rich lipoprotein levels. In conclusion, omega-3 fatty acids are currently being evaluated in large CV outcome studies in statin-treated patients; these studies should help to elucidate the causative role of triglycerides in atherosclerotic CV disease.

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“…Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors represent a new class of monoclonal antibodies to lower LDL cholesterol levels that have been introduced into clinical use recently (Alkindi et al, ). A number of guidelines recommend the addition of fibrates, niacin, or long‐chain omega‐3 fatty acids if elevated triglyceride or non‐HDL cholesterol levels persist despite the use of high‐intensity statin therapy (Ito, ). However, ezetimibe is the only nonstatin shown to reduce atherosclerotic CVD events when added to a statin.…”

Section: Introductionmentioning

confidence: 99%

Major pathogenic mechanisms in vascular dementia: Roles of cellular stress response and hormesis in neuroprotection

Calabrese

Giordano

Signorile

et al. 2016

J of Neuroscience Research

125

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Vascular dementia (VaD), considered the second most common cause of cognitive impairment after Alzheimer disease in the elderly, involves the impairment of memory and cognitive function as a consequence of cerebrovascular disease. Chronic cerebral hypoperfusion is a common pathophysiological condition frequently occurring in VaD. It is generally associated with neurovascular degeneration, in which neuronal damage and blood-brain barrier alterations coexist and evoke beta-amyloid-induced oxidative and nitrosative stress, mitochondrial dysfunction, and inflammasome- promoted neuroinflammation, which contribute to and exacerbate the course of disease. Vascular cognitive impairment comprises a heterogeneous group of cognitive disorders of various severity and types that share a presumed vascular etiology. The present study reviews major pathogenic factors involved in VaD, highlighting the relevance of cerebrocellular stress and hormetic responses to neurovascular insult, and addresses these mechanisms as potentially viable and valuable as foci of novel neuroprotective methods to mitigate or prevent VaD. © 2016 Wiley Periodicals, Inc.

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Long-chain omega-3 fatty acids, fibrates and niacin as therapeutic options in the treatment of hypertriglyceridemia: A review of the literature

Cited by 55 publications

References 96 publications

Silence of lncRNA UCA1 Represses the Growth and Tube Formation of Human Microvascular Endothelial Cells Through miR-195

Silence of lncRNA UCA1 Represses the Growth and Tube Formation of Human Microvascular Endothelial Cells Through miR-195

Triglycerides and Triglyceride-Rich Lipoproteins in the Causal Pathway of Cardiovascular Disease

Major pathogenic mechanisms in vascular dementia: Roles of cellular stress response and hormesis in neuroprotection

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