Apolipoprotein(a) is the Product of a Pseudogene: Implications for the Pathophysiology of Lipoprotein(a)

Sloop, Gregory D.; Pop, Gheorghe; Weidman, Joseph J; Cyr, John A. St.

doi:10.7759/cureus.2715

Cited by 2 publications

(2 citation statements)

References 43 publications

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“…Interestingly, we found that most genes of the top 30 MDG differentially 5hmC markers were pseudogenes. The experimental data obtained during recent years indicate this understanding of the nature of pseudogenes is not entirely correct, and many pseudogenes are functionally significant elements of the genome and may play a regulatory role in the form of non-coding RNA [57][58][59]. Thus, we speculated that 5hmC regulated gene expression by regulating the production of pseudogene RNA.…”

Section: Discussionmentioning

confidence: 97%

5-Hydroxymethylcytosine signatures in circulating cell-free DNA as diagnostic and predictive biomarkers for coronary artery disease

et al. 2020

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Background: The 5-hydroxymethylcytosine (5hmC) DNA modification is an epigenetic marker involved in a range of biological processes. Its function has been studied extensively in tumors, neurodegenerative diseases, and atherosclerosis. Studies have reported that 5hmC modification is closely related to the phenotype transformation of vascular smooth muscle cells and endothelial dysfunction. However, its role in coronary artery disease (CAD) has not been fully studied. Results: To investigate whether 5hmC modification correlates with CAD pathogenesis and whether 5hmC can be used as a biomarker, we used a low-input whole-genome sequencing technology based on selective chemical capture (hmC-Seal) to firstly generate the 5hmC profiles in the circulating cell-free DNA(cfDNA) of CAD patients, including stable coronary artery disease (sCAD) patients and acute myocardial infarction (AMI) patients. We detected a significant difference of 5hmC enrichment in gene bodies from CAD patients compared with normal coronary artery (NCA) individuals. Our results showed that CAD patients can be well separated from NCA individuals by 5hmC markers. The prediction performance of the model established by differentially regulated 5hmc modified genes were superior to common clinical indicators for the diagnosis of CAD (AUC = 0.93) and sCAD (AUC = 0.93). Specially, we found that 5hmC markers in cfDNA showed prediction potential for AMI (AUC = 0.95), which was superior to that of cardiac troponin I, muscle/brain creatine kinase, and myoglobin. Conclusions: Our results suggest that 5hmC markers derived from cfDNA can serve as effective epigenetic biomarkers for minimally noninvasive diagnosis and prediction of CAD.

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Section: Discussionmentioning

confidence: 97%

5-Hydroxymethylcytosine signatures in circulating cell-free DNA as diagnostic and predictive biomarkers for coronary artery disease

et al. 2020

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“…A 2010 review concluded that elevated Lp(a) was a cause of premature atherosclerosis [80]. We have recently argued that Lp(a) causes disease by increasing blood viscosity [81]. Supporting this, Bohl, et al performed a single session of lipoprotein apheresis, which removes both LDL and Lp(a), in ten subjects with Lp(a) levels > 60 mg/dL.…”

Section: Lipoprotein(a)mentioning

confidence: 99%

Why Atherothrombosis is in Principle a Hematologic Disease: The Effect of Disorders and Drugs which Affect Thrombosis on the Development of Atherosclerotic Plaques

D¹,

Gheorghe²,

J³

et al. 2018

Int Arch Cardiovasc Dis

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The authors hypothesize that thrombosis causes both the complications of atherosclerosis as well as the underlying lesion, the atherosclerotic plaque. Atherosclerotic plaques develop from the organization of mural thrombi. In this process, circulating progenitor cells trapped within the thrombus differentiate into myofibroblasts which synthesize collagen, and endothelial cells which form granulation tissue. Eventually, all or most of the thrombus is replaced by collagen. Thus, conditions and drugs which affect thrombosis also affect the development of atherosclerotic plaques, i.e., atherogenesis. The authors review the process of organization and evidence showing that altered hemodynamics, increased blood viscosity, thrombophilias, coagulopathies, myeloproliferative disorders and drugs which modify the risk of thrombosis also affect atherogenesis. Accelerated atherogenesis is an underappreciated complication of many of these conditions. This paradigm explains how diverse risk factors, many of which have no association with inflammation or dyslipidemia, cause the same lesion. These data have implications for atherothrombosis theory and clinical practice.

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Apolipoprotein(a) is the Product of a Pseudogene: Implications for the Pathophysiology of Lipoprotein(a)

Cited by 2 publications

References 43 publications

5-Hydroxymethylcytosine signatures in circulating cell-free DNA as diagnostic and predictive biomarkers for coronary artery disease

5-Hydroxymethylcytosine signatures in circulating cell-free DNA as diagnostic and predictive biomarkers for coronary artery disease

Why Atherothrombosis is in Principle a Hematologic Disease: The Effect of Disorders and Drugs which Affect Thrombosis on the Development of Atherosclerotic Plaques

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