Protein changes in non-LDL-lipoproteins in familial hypercholesterolemia: implications in cardiovascular disease manifestation and outcome

Badimon, Lina; Padró, Teresa; Cubedo, Judit

doi:10.1097/mol.0000000000000441

Cited by 7 publications

(3 citation statements)

References 48 publications

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“…Additionally platelets can modify native HDL, resulting in a dysfunctional and pro-thrombotic form ( Blache et al, 2012 ). Patients with familiar hypercholesterolemia display reduced concentrations of apoAIV and LCAT and a truncated form of apoLI ( Cubedo et al, 2016 ; Badimon et al, 2017 ). Experimental studies showed that much of the structural modifications and impairment in HDL function are as a result of increased LDL cholesterol (LDL-C) concentrations ( Vilahur et al, 2015 ; Padró et al, 2017 ).…”

Section: Hdl Functionalitymentioning

confidence: 99%

Pharmacological Intervention to Modulate HDL: What Do We Target?

et al. 2018

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The cholesterol concentrations of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) have traditionally served as risk factors for cardiovascular disease. As such, novel therapeutic interventions aiming to raise HDL cholesterol have been tested in the clinical setting. However, most trials led to a significant increase in HDL cholesterol with no improvement in cardiovascular events. The complexity of the HDL particle, which exerts multiple physiological functions and is comprised of a number of subclasses, has raised the question as to whether there should be more focus on HDL subclass and function rather than cholesterol quantity. We review current data regarding HDL subclasses and subclass-specific functionality and highlight how current lipid modifying drugs such as statins, cholesteryl ester transfer protein inhibitors, fibrates and niacin often increase cholesterol concentrations of specific HDL subclasses. In addition this review sets out arguments suggesting that the HDL3 subclass may provide better protective effects than HDL2.

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Section: Hdl Functionalitymentioning

confidence: 99%

Pharmacological Intervention to Modulate HDL: What Do We Target?

et al. 2018

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“…Recent reviews have critically addressed the role of high-density lipoprotein (HDL) in atherosclerosis development, highlighting the potential rapid movement of unesterified cholesterol (UC) from cells and triglyceride-rich particles to HDL as well as from HDL to LDL or tissues [4,5]. There is also evidence indicating that HDL remodeling, metabolism, and function, including its ability to induce macrophage cholesterol efflux, are impaired in the monogenic forms of FH [6][7][8][9][10]. Whether this impairment is intrinsic to the disease and influences the entire reverse cholesterol transport (RCT) pathway and cardiovascular risk and is corrected by current treatments is not yet well-established.…”

Section: Abbreviationsmentioning

confidence: 99%

“…Indeed, HDL composition is a key atheroprotective determinant. Decreased levels of HDL-cholesterol (HDL-C) have been consistently observed in both heterozygous FH and homozygous FH in association with HDL structural and functional abnormalities [6][7][8][9][10].…”

Section: Hdl Content and Remodeling Alterations In Fhmentioning

confidence: 99%