Lipoprotein (a)—We Know So Much Yet Still Have Much to Learn …

Banach, Maciej

doi:10.1161/jaha.116.003597

Cited by 40 publications

(23 citation statements)

References 18 publications

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“…It is also possible that abnormal Mon2 NFjB and phagocytic activity may reflect other, currently unacknowledged beneficial functions of Mon2 and related regulatory pathways [20][21][22]. These might include roles in angiogenesis, modulation of myofibroblast function and extracellular matrix…”

Section: Discussionmentioning

confidence: 99%

Mon2 predicts poor outcome in ST‐elevation myocardial infarction

et al. 2019

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Aims There are limited data on the role of human monocyte subsets in ST‐elevation myocardial infarction (STEMI). The study aimed to establish the relationship between monocyte subsets, their phagocytic and nuclear factor κB (NFκB) activity and outcomes in STEMI. Methods Monocyte subsets and their phagocytic activity and intracellular levels of inhibitory κB kinase β (IKKβ, marker of NFκB activity) were measured by flow cytometry in 245 patients with STEMI, median follow‐up of 46 months. Results Mon2 (CD14++CD16+CCR2+) counts were independently predictive of major adverse cardiovascular events (MACE) [4th quartile HR 3.42 (95% CI 1.43–8.16), P = 0.006 and 3rd quartile HR 2.88 (95% CI 1.19–7.00), P = 0.02 vs. 1st quartile]. Mon2 subset was the only subset associated with higher occurrence of heart failure (4th quartile vs. 1st quartile, sevenfold, P = 0.001 on univariate analysis; fivefold, P = 0.04 on multivariable analysis). On receiver operating characteristic, analysis including of Mon2 improved prognostic value of troponin T and creatine kinase for MACE and heart failure (HF). Higher intracellular Mon2 IKKβ levels were associated with 10‐fold lower occurrence of HF on multivariable analysis (4th vs. 1st quartiles, P = 0.03). Abnormal Mon1 and Mon2 phagocytic capacities were related to HF development, but the association was dependent on the infarct size and other prognosticators. High Mon2 levels were associated with lower ejection fraction after STEMI onset (P = 0.001) and at 6‐month follow‐up (P < 0.001). Conclusions Abnormal Mon2 characteristics have a unique association with poor outcome in patients with STEMI. The relation of Mon2 with occurrence of HF is strongly and independently related to their functional status, which may have potential therapeutic implications.

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Section: Discussionmentioning

confidence: 99%

Mon2 predicts poor outcome in ST‐elevation myocardial infarction

et al. 2019

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“…We showcase the application of MR-Base through a systematic MR study of the effect of LDL cholesterol, lipoprotein(a) [Lp(a)] and triglycerides-intervention targets for the prevention of coronary heart disease (CHD)-on a range of health-related outcomes. First, We perform MR analyses to predict the efficacy 20 and safety 21,22 of emerging lipid-lowering drugs 23,24 . Second, to gain insights into the broad safety of lipid-targeted interventions, we perform MR analyses of lipids against a wide range of disease outcomes and related traits.…”

Section: Introductionmentioning

confidence: 99%

MR-Base: a platform for systematic causal inference across the phenome using billions of genetic associations

Hemani

Zheng

Wade

et al. 2016

Preprint

185

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Published genetic associations can be used to infer causal relationships between phenotypes, bypassing the need for individual-level genotype or phenotype data. We have curated complete summary data from 1094 genome-wide association studies (GWAS) on diseases and other complex traits into a centralised database, and developed an analytical platform that uses these data to perform Mendelian randomization (MR) tests and sensitivity analyses (MR-Base, http://www.mrbase.org). Combined with curated data of published GWAS hits for phenomic measures, the MR-Base platform enables millions of potential causal relationships to be evaluated. We use the platform to predict the impact of lipid lowering on human health. While our analysis provides evidence that reducing LDL-cholesterol, lipoprotein(a) or triglyceride levels reduce coronary disease risk, it also suggests causal effects on a number of other non-vascular outcomes, indicating potential for adverse-effects or drug repositioning of lipid-lowering therapies.

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“…It has been shown that Lp(a) contributes to atherosclerosis through accelerated transport of oxidized phospholipids [2] and inhibition of fibrinolysis [3]. Plasma Lp(a) levels are influenced by several factors such as genetic polymorphisms of apo(a) [4], sex, age, race [5, 6], smoking, alcohol consumption, dietary habits, intense exercise, thyroid function [7] and hormonal factors.…”

Section: Introductionmentioning

confidence: 99%

The Effects of Tamoxifen on Plasma Lipoprotein(a) Concentrations: Systematic Review and Meta-Analysis

Sahebkar

Şerban

Penson

et al. 2017

Drugs

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IntroductionTamoxifen is a selective estrogen receptor modulator widely used in the treatment of breast cancer. Tamoxifen therapy is associated with lower circulating low-density lipoprotein cholesterol and increased triglycerides, but its effects on other lipids are less well studied.AimsWe aimed to investigate the effect of tamoxifen on circulating concentrations of lipoprotein(a) [Lp(a)] through a meta-analysis of available randomized controlled trials (RCTs) and observational studies.MethodsThis study was registered in the PROSPERO database (CRD42016036890). Scopus, MEDLINE and EMBASE were searched from inception until 22 March 2016 to identify studies investigating the effect of tamoxifen on Lp(a) values in humans. Meta-analysis was performed using an inverse variance-weighted, random-effects model with standardized mean difference (SMD) as the effect size estimate.ResultsMeta-analysis of five studies with 215 participants suggested a statistically significant reduction of Lp(a) levels following tamoxifen treatment (SMD −0.41, 95% confidence interval −0.68 to −0.14, p = 0.003). This effect was robust in the sensitivity analysis.ConclusionsMeta-analysis suggested a statistically significant reduction of Lp(a) levels following tamoxifen treatment. Further well-designed trials are required to validate these results.

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Lipoprotein (a)—We Know So Much Yet Still Have Much to Learn …

Cited by 40 publications

References 18 publications

Mon2 predicts poor outcome in ST‐elevation myocardial infarction

Mon2 predicts poor outcome in ST‐elevation myocardial infarction

MR-Base: a platform for systematic causal inference across the phenome using billions of genetic associations

The Effects of Tamoxifen on Plasma Lipoprotein(a) Concentrations: Systematic Review and Meta-Analysis

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