ApoCIII as a Cardiovascular Risk Factor and Modulation by the Novel Lipid-Lowering Agent Volanesorsen

Rocha, Natália A.; East, Cara; Zhang, Jun; McCullough, Peter A.

doi:10.1007/s11883-017-0697-3

Cited by 45 publications

(24 citation statements)

References 91 publications

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“…28 There are also data from genetic gain -of -function apo C3 mutations and clinical studies with apo C3 inhibition indicating that this apo is associated with incident cardiovascular disease. 29,30 Besides its effects on lipid and lipoprotein metabolism, apo C3 is directly involved in stimulation of vascular inflammatory processes. There are data indicating that apo C3 directly provokes proinflammatory responses in vascular cells, including monocytes and endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Serum pentraxin 3 concentration in patients with type 2 diabetes mellitus and non-alcoholic fatty liver disease

Trojak¹,

Waluś-Miarka²,

Kapusta³

et al. 2019

Polish Archives of Internal Medicine

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INTRODUCTION Nonalcoholic fatty liver disease (NAFLD) is common in patients with type 2 diabetes (T2D). Pentraxin 3 (PTX3), a marker of inflammation, is a cardiovascular risk factor. OBJECTIVES We examined clinical and biochemical factors associated with serum PTX3 concentrations in patients with T2D with and without NAFLD. PATIENTS AND METHODS Serum material was obtained from 116 patients with T2D (mean age, 59.1 years), including 79 patients with NAFLD. RESULTS Median (interquartile range) PTX3 level was 4.264 (2.293) ng/ml in patients with and 3.773 (3.223) ng/ml in patients without NAFLD (P = 0.93). In the whole group, PTX3 level was associated with total cholesterol, low-density lipoprotein cholesterol (LDL-C), apolipoprotein (apo) B100, apo C3, triglyceride (TG) concentrations, and waist circumference after adjustment for age and gender. As indicated by partial regression coefficient b, increase of independent variable LDL-C by 1 mmol/l was associated with the rise of PTX3 by 1.2017 ng/ml, increase of apo B100 by 1 mg/dl with the rise of PTX3 by 1.0051 ng/ml, and increase of apo C3 by 1 µg/dl with the rise of PTX3 by 1.0012 ng/ml. In patients with T2D with NAFLD, total cholesterol, LDL-C, TG, apo C3, and apo B100 were associated with PTX3. Associations of PTX3 with apolipoproteins were observed only in the NAFLD group. CONCLUSIONS Reported associations of PTX3 level add new insight into possible mechanisms of its atherogenic actions.

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Section: Discussionmentioning

confidence: 99%

Serum pentraxin 3 concentration in patients with type 2 diabetes mellitus and non-alcoholic fatty liver disease

Trojak¹,

Waluś-Miarka²,

Kapusta³

et al. 2019

Polish Archives of Internal Medicine

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“…As such, CETP inhibition via monoclonal antibodies, vaccines, and antisense oligonucleotides remains of major clinical interest (Shrestha et al, 2018). There are numerous emerging therapies including icosapent-etyhl (Bhatt et al, 2017), bempedoic acid (Pinkosky et al, 2016;Ray et al, 2019), Apo C-III (a key regulator in hypertriglyceridemia) inhibition (Rocha et al, 2017) and novel cellular binding proteins (Maqbool et al, 2015), that are being studied as tailored tools to combat dyslipidemia-their effect in the CKD population has yet to be determined. A brief summary of hyperlipidemic treatment options (including a few therapies not mentioned above) is provided in Table. 2 (Einarsson et al, 1991;Fares et al, 2014;Grundy et al, 2018;Kamanna and Kashyap, 2008;KDIGO, 2013;Ray et al, 2019;Shearer et al, 2012).…”

Section: Proprotein Convertase Subtilisin/kexin Type 9 (Pcsk9) Inhibimentioning

confidence: 99%

Alteration of lipid metabolism in chronic kidney disease, the role of novel antihyperlipidemic agents, and future directions

Sudhakaran

Tecson

Kluger

et al. 2018

Rev. Cardiovasc. Med.

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The role of anti-hyperlipidemic therapy remains of key importance in the treatment of atherosclerotic disease. Moreover, given an already exaggerated predisposition for vascular disease at baseline, there is a preponderance of data that show management of hyperlipidemia is especially important in patients with chronic kidney disease. This is a concise, up-to-date review of lipid physiology, alterations in lipid concentrations with progressive renal failure, and currently available and emerging hyperlipidemic treatment options. Specifically, the roles of these therapies in patients with chronic kidney disease are reviewed.

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“…The pathogenesis of diabetic dyslipidemia has been ascribed to abnormalities in the quantity, quality, and kinetics of lipoprotein. [14][15][16] Quantitative derangements include an increase in triglyceride levels and a decrease in HDL cholesterol levels. Qualitative abnormalities include a higher participation of large very low-density lipoprotein (VLDL) 1, small density LDL particles, triglyceride-rich VLDL 1, and triglyceride-rich HDL 2, and kinetic abnormalities include an increased production of VLDL 1, decreased VLDL catabolism, and increased HDL catabolism.…”

Section: Pathophysiology Of Diabetic Dyslipidemiamentioning

confidence: 99%

“…Diabetic dyslipidemia is characterized by elevated LDL cholesterol, the predominance of small density LDL particles, elevated triglycerides, and decreased HDL cholesterol. 14 The primary goal of the pharmacological management of diabetic dyslipidemia is to reduce the levels of LDL cholesterol, and the secondary goal focuses on reducing non-HDL cholesterol and Apo B levels. 4 To further reduce cardiovascular risk, management should include attempts to decrease triglycerides and increase HDL cholesterol.…”

Section: Clinical Phase 3 Trials In Patients With Type 2 Diabetes Witmentioning

confidence: 99%

Usefulness of alirocumab and evolocumab for the treatment of patients with diabetic dyslipidemia

Zhang

Tecson

Rocha

et al. 2018

Baylor University Medical Center Proceedings

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In 2015, the US Food and Drug Administration (FDA) approved the anti-proprotein convertase subtilsin/kexin type 9 (PCSK9) monoclonal antibodies, alirocumab and evolocumab, to treat patients with hypercholesterolemia and mixed dyslipidemia. Since then, considerable attention has been paid to the use of these monoclonal antibodies for the treatment of diabetic dyslipidemia with a goal of reducing the risk for cardiovascular disease. Recently, consensus statements on the clinical use of PCSK9 inhibitors in patients with type 2 diabetes mellitus, who are unable to achieve the goal of low-density lipoprotein cholesterol (<70 mg/dL or <1.8 mmol/L), have been published by panels of experts in Greece, Europe (European Society of Cardiology and European Atherosclerosis Society Task Force), and the United States (American College of Cardiology Consensus Committee). On December 1, 2017, the FDA approved evolocumab to prevent heart attack, stroke, and coronary revascularization. In this article, we review recent advances concerning the pathophysiology of diabetic dyslipidemia, the physiology of PCSK9, the mechanisms of action of PCSK9 inhibitors, clinical trials examining PCSK9 inhibitors in type 2 diabetes, and perspectives of nonstatin therapy in the treatment of diabetic dyslipidemia.

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ApoCIII as a Cardiovascular Risk Factor and Modulation by the Novel Lipid-Lowering Agent Volanesorsen

Cited by 45 publications

References 91 publications

Serum pentraxin 3 concentration in patients with type 2 diabetes mellitus and non-alcoholic fatty liver disease

Serum pentraxin 3 concentration in patients with type 2 diabetes mellitus and non-alcoholic fatty liver disease

Alteration of lipid metabolism in chronic kidney disease, the role of novel antihyperlipidemic agents, and future directions

Usefulness of alirocumab and evolocumab for the treatment of patients with diabetic dyslipidemia

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