Lipoprotein(a) and inflammation: A dangerous duet leading to endothelial loss of integrity

Pirro, Matteo; Bianconi, Vanessa; Paciullo, Francesco; Mannarino, Massimo Raffaele; Bagaglia, Francesco; Sahebkar, Amirhossein

doi:10.1016/j.phrs.2017.02.001

Cited by 59 publications

(46 citation statements)

References 114 publications

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“…Lipoprotein (a) has proatherogenic and prothrombotic effects. 45 Lipoprotein (a) promotes the expression of pro-inflammatory cytokines and induces endothelial dysfunction. 46 Elevation of lipoprotein (a) and low-grade inflammation commonly coexist, and both play deleterious roles on endothelial integrity, at both the functional and structural levels.…”

Section: Discussionmentioning

confidence: 99%

Effect of Rosuvastatin on Cholesterol Efflux Capacity and Endothelial Function in Type 2 Diabetes Mellitus and Dyslipidemia

Jung

Kim

Han³

et al. 2018

Circ J

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Section: Discussionmentioning

confidence: 99%

Effect of Rosuvastatin on Cholesterol Efflux Capacity and Endothelial Function in Type 2 Diabetes Mellitus and Dyslipidemia

Jung

Kim

Han³

et al. 2018

Circ J

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“…Oxidized phospholipids (OxPLs) play a fundamental role in the early stages of atherosclerosis; they elicit robust proinflammatory responses in murine macrophages and monocytes and are capable of stimulating proinflammatory genes, leading to vascular inflammation [73]. Several studies have reported that OxPLs usually form on oxidizing LDL-C and apoptotic cell membranes and are released into circulation a erward [74][75][76].…”

Section: Binding and Carrying Of Oxidized Phospholipids And Lp-pla2mentioning

confidence: 99%

“…lipoproteins [94]. Subsequently, OxLp(a) triggers a sequence of pro-inflammatory events leading to the development and progression of atherosclerosis [73,95]. OxLp(a) is then trapped within the intimal layer of the injured vessel, leading to its degradation by lipoprotein lipase, which liberates free fatty acids and monoacylglycerols, resulting in even more local inflammation [73].…”

Section: The Pathogenicity Of Lp(a)mentioning

confidence: 99%

“…Subsequently, OxLp(a) triggers a sequence of pro-inflammatory events leading to the development and progression of atherosclerosis [73,95]. OxLp(a) is then trapped within the intimal layer of the injured vessel, leading to its degradation by lipoprotein lipase, which liberates free fatty acids and monoacylglycerols, resulting in even more local inflammation [73]. It is worth mentioning that the diacylated and triacylated lipoproteins can be identified by Toll-like receptors (TLR-4) and pattern-recognition receptors (PPRs), which usually respond to attacking microorganisms and activate the inflammatory response [73,[96][97][98].…”

Section: The Pathogenicity Of Lp(a)mentioning

confidence: 99%

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Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule

2020

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Lipoprotein(a) [Lp(a)], aka “Lp little a”, was discovered in the 1960s in the lab of the Norwegian physician Kåre Berg. Since then, we have greatly improved our knowledge of lipids and cardiovascular disease (CVD). Lp(a) is an enigmatic class of lipoprotein that is exclusively formed in the liver and comprises two main components, a single copy of apolipoprotein (apo) B-100 (apo-B100) tethered to a single copy of a protein denoted as apolipoprotein(a) apo(a). Plasma levels of Lp(a) increase soon after birth to a steady concentration within a few months of life. In adults, Lp(a) levels range widely from <2 to 2500 mg/L. Evidence that elevated Lp(a) levels >300 mg/L contribute to CVD is significant. The improvement of isoform-independent assays, together with the insight from epidemiologic studies, meta-analyses, genome-wide association studies, and Mendelian randomization studies, has established Lp(a) as the single most common independent genetically inherited causal risk factor for CVD. This breakthrough elevated Lp(a) from a biomarker of atherosclerotic risk to a target of therapy. With the emergence of promising second-generation antisense therapy, we hope that we can answer the question of whether Lp(a) is ready for prime-time clinic use. In this review, we present an update on the metabolism, pathophysiology, and current/future medical interventions for high levels of Lp(a).

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“…The link between inflammation and plasma Lp(a) level has been extensively investigated in recent years, resulting in the final conclusion that Lp(a) may act both as positive and negative acute phase reactant (Pirro et al, ). Intriguingly, the interleukin‐6 receptor (IL‐6R) blocker tocilizumab reduced inflammatory disease activity in rheumatoid arthritis patients and plasma Lp(a) levels as well (McInnes et al, ).…”

Section: Therapeutic Modalities To Interfere With Lp(a)mentioning

confidence: 99%

Lipoprotein(a): A missing culprit in the management of athero‐thrombosis?

Ferretti

Bacchetti

Johnston

et al. 2017

Journal Cellular Physiology

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Lipoprotein(a) Lp(a) is a cholesterol-rich, LDL-like particle that is independently associated with an increased risk for ischemic heart disease, atherosclerosis, thrombosis, and stroke. Genetic variation in the Lp(a) locus and some other genes related to Lp(a) synthesis and metabolism play a critical role in regulating plasma Lp(a) levels. The pathophysiological potential of Lp(a) is related to proatherogenic and prothrombotic effects on the vasculature. Different molecular mechanisms underlying the atherothrombotic potential of Lp(a), free apolipoprotein(a), and oxidized-Lp(a) have been proposed. However, plasma Lp(a) assay is complicated by problems associated with quantification and standardization owing to the polymorphic nature of this lipoprotein. This review has focused on the physicochemical properties of Lp(a), the genetic aspects of Lp(a), the need for accurate determination of Lp(a), the synthesis, and recent findings on metabolism of Lp(a). Lastly, the patho-physiological mechanisms by which Lp(a) may increase athero-thrombosis and an overview on the therapeutic modalities to interfere with Lp(a) are summarized.

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Lipoprotein(a) and inflammation: A dangerous duet leading to endothelial loss of integrity

Cited by 59 publications

References 114 publications

Effect of Rosuvastatin on Cholesterol Efflux Capacity and Endothelial Function in Type 2 Diabetes Mellitus and Dyslipidemia

Effect of Rosuvastatin on Cholesterol Efflux Capacity and Endothelial Function in Type 2 Diabetes Mellitus and Dyslipidemia

Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule

Lipoprotein(a): A missing culprit in the management of athero‐thrombosis?

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