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| http://dx.doi.org/10.1016/j.amjcard.2025.03.022 | DOI Listing |
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Electronegative LDL strongly induces LRP1 release from human monocytes and macrophages.
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Background: Electronegative LDL (LDL(-)) is a circulant modified LDL with inflammatory properties whose proportion raises in ischemic events. The soluble form of LDL receptor related protein 1 (sLRP1) increases in blood in pathological situations, including ischemic stroke. We aimed to evaluate the effect of LDL(-) on sLRP1 release from monocytes and macrophages.
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Turk Kardiyol Dern Ars
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Department of Cardiology, Koç University School of Medicine, Istanbul, Türkiye.
Objective: Coronary artery calcification (CAC) and osteoporosis are common age-related conditions that may share underlying mechanisms such as inflammation and lipid dysregulation. Lipoprotein(a) [Lp(a)] has been suggested as a potential contributor to both processes. This study aims to investigate the relationship between CAC, bone mineral density (BMD), and Lp(a) levels in a statin-naive elderly population.
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Am J Prev Cardiol
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Division of Cardiovascular Medicine, University of California San Diego, La Jolla, CA, USA.
Elevated lipoprotein(a) [Lp(a)] is well established as a common risk factor for atherosclerotic cardiovascular disease (ASCVD). Lp(a) levels are >90 % genetically determined. However, Lp(a) remains very underrecognized as a cardiovascular risk factor with low rates of testing.
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Eur Heart J
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Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy.
Cardiovascular disease remains a major global health challenge, with dyslipidaemia being a key modifiable risk factor. While low density lipoprotein cholesterol (LDL-C) is the primary target for lipid-lowering therapies, recent evidence highlights the importance of triglycerides, apolipoprotein B (apoB), and lipoprotein(a) [Lp(a)] for residual cardiovascular risk. Current lipid-lowering therapies target key enzymes and proteins involved in cholesterol and lipid metabolism.
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Eur Heart J Open
July 2025
Amsterdam UMC Location University of Amsterdam, Department of Experimental Vascular Medicine, Amsterdam Cardiovascular Sciences, Meibergdreef 9, 1105AZ Amsterdam, Netherlands.
Aims: Calcific aortic valve disease is the most common valvular heart disease characterized by an inflammatory response in the leaflets followed by fibro-calcific remodelling of valvular interstitial cells (VICs). Lipoprotein(a) [Lp(a)] is a well-recognized risk factor for CAVD, however the role of metabolism in driving Lp(a)-induced inflammation remains largely elusive. Therefore, we aim to investigate the role of Lp(a) in driving inflammatory and metabolic changes in VICs and examine how alterations in cellular metabolism can alter their inflammatory phenotype.
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