Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Pharmacogenomics: Identification of New Drug Targets01:29

Pharmacogenomics: Identification of New Drug Targets

Advances in genomics have profoundly influenced drug discovery by increasing both the speed and accuracy of pharmaceutical development. Pharmacogenomics, which examines how genetic variation influences drug response, facilitates the identification of novel therapeutic targets and enables patient stratification for personalized treatment. These strategies contribute to improved drug efficacy, minimized adverse effects, and more efficient clinical trial design.Mapping genetic differences...
Pharmacogenetics of Drug Transporters: P-Glycoprotein and Solute Carrier Transporters01:16

Pharmacogenetics of Drug Transporters: P-Glycoprotein and Solute Carrier Transporters

The pharmacogenetics of drug transporters is increasingly recognized as a critical factor influencing interindividual variability in drug absorption, distribution, and elimination. These membrane-bound proteins regulate drugs' movement across cellular barriers by actively pumping them out (efflux) or facilitating their uptake (influx). Among the major transporter families, ATP-binding cassette (ABC) and solute carrier (SLC) transporters play particularly prominent roles. Genetic polymorphisms...
Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu01:29

Pharmacogenetic Phenotypes: Alterations in Pharmacokinetics, Drug Targets and Biologic Milieu

Genetic variations significantly influence drug response through pharmacokinetics, receptor interactions, and biologic milieu modifications. Pharmacokinetic alterations impact drug metabolism and clearance, affecting efficacy and toxicity. Variants in drug-metabolizing enzymes, such as CYP2C9 and CYP2C19, alter drug activation and elimination. For example, CYP2C9 loss-of-function variants require lower warfarin doses to prevent excessive bleeding, while CYP2C19 variants reduce clopidogrel...
Atherosclerosis III: Management01:26

Atherosclerosis III: Management

Management of atherosclerosis involves an integrated strategy encompassing pharmacological treatment, surgical interventions, lifestyle changes, and nutrition therapy to address the multifactorial nature of the disease.Pharmacological TherapyA cornerstone of atherosclerosis management is the use of pharmacological agents. Statins, such as atorvastatin, are pivotal in inhibiting HMG-CoA reductase, an enzyme that catalyzes an initial step in cholesterol synthesis in the liver. This reduction in...
Lipid-Lowering Drugs: Statins and Miscellaneous Agents01:20

Lipid-Lowering Drugs: Statins and Miscellaneous Agents

Hyperlipidemia, a medical condition often referred to as high cholesterol, is characterized by abnormally elevated levels of lipids in the bloodstream. When present in excess, these lipids, specifically cholesterol and triglycerides, can lead to serious health complications, often involving cardiovascular diseases. Illnesses like atherosclerosis, heart attacks, and pancreatitis have all been linked to untreated hyperlipidemia. This means controlling and regulating cholesterol and triglyceride...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Time-dependent lipid profile inversely associates with mortality in hemodialysis patients - independent of inflammation/malnutrition.

Journal of internal medicine·2021
Same author

Association of mitochondrial DNA copy number with metabolic syndrome and type 2 diabetes in 14 176 individuals.

Journal of internal medicine·2021
Same author

Mitochondrial DNA copy number is associated with all-cause mortality and cardiovascular events in patients with peripheral arterial disease.

Journal of internal medicine·2020
Same author

Acupuncture point injection treatment of primary dysmenorrhoea: a randomised, double blind, controlled study.

BMJ open·2016
Same author

Telomere length increase after weight loss induced by bariatric surgery: results from a 10 year prospective study.

International journal of obesity (2005)·2015
Same author

Geographically predominant genotypes of Aspergillus terreus species complex in Austria: s microsatellite typing study.

Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases·2015
Same journal

Patients with hereditary hemorrhagic telangiectasia have significantly reduced overall survival-And likely by a greater magnitude than we realize.

Journal of internal medicine·2026
Same journal

Social jet lag is associated with incident cardiovascular disease independent of sleep duration and cardiac genetic risk.

Journal of internal medicine·2026
Same journal

Multicenter validation of a severity index model for predicting postoperative acute kidney injury.

Journal of internal medicine·2026
Same journal

The changing epidemiology of human type 2 diabetes-associated atherosclerosis: Pathophysiological mechanisms and emerging treatment possibilities.

Journal of internal medicine·2026
Same journal

Angiopoietin-like protein 3 complete and partial deficiency markedly accelerates apolipoprotein B48 and B100 metabolism in triglyceride-rich lipoproteins in humans.

Journal of internal medicine·2026
Same journal

Authors' reply: Myasthenia gravis following the initiation of statin therapy.

Journal of internal medicine·2026
See all related articles

Related Experiment Video

Updated: May 18, 2026

Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
06:47

Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation

Published on: January 28, 2021

Lipoprotein(a): resurrected by genetics.

F Kronenberg1, G Utermann

  • 1Division of Genetic Epidemiology, Innsbruck Medical University, Innsbruck, Austria.

Journal of Internal Medicine
|September 25, 2012
PubMed
Summary
This summary is machine-generated.

Lipoprotein(a) [Lp(a)], a genetic risk factor for coronary heart disease (CHD), is influenced by LPA gene variants. Low kringle IV copy numbers in the LPA gene significantly elevate CHD risk, highlighting Lp(a) as a critical cardiovascular risk factor.

Related Experiment Videos

Last Updated: May 18, 2026

Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
06:47

Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation

Published on: January 28, 2021

Area of Science:

  • Cardiovascular Genetics
  • Lipid Metabolism
  • Genetic Epidemiology

Background:

  • Plasma lipoprotein(a) [Lp(a)] is a major genetic risk factor for coronary heart disease (CHD).
  • Lp(a) levels are primarily determined by genetic variants at the LPA locus.
  • The association between Lp(a) and CHD risk is supported by extensive genetic evidence.

Purpose of the Study:

  • To summarize the genetic basis of Lp(a) and its role in coronary heart disease.
  • To explore the mechanisms underlying Lp(a) pathogenicity.
  • To review the impact of Lp(a)-lowering therapies on cardiovascular outcomes.

Main Methods:

  • Genetic association studies analyzing the LPA locus and kringle IV copy number variation.
  • Review of studies investigating Lp(a) pathogenicity mechanisms, including oxidized phospholipid binding.
  • Analysis of clinical trials and proof-of-principle studies on Lp(a)-lowering interventions.

Main Results:

  • Copy number variation in the kringle IV domain of the LPA gene is strongly linked to Lp(a) levels and CHD risk.
  • Alleles with low kringle IV copy numbers (25-35% population frequency) double the relative risk for CHD events.
  • Oxidized phospholipids binding to Lp(a) is a potential mechanism for its pathogenicity.
  • While some Lp(a)-lowering drugs have pleiotropic effects, direct cardiovascular outcome improvements are pending.
  • Apheresis to lower very high Lp(a) in high-risk patients significantly reduced major coronary events in a proof-of-principle study.

Conclusions:

  • Genetic variants in the LPA gene, particularly kringle IV copy number, are key determinants of plasma Lp(a) levels and CHD risk.
  • Lp(a) represents a potent, genetically determined risk factor for cardiovascular disease.
  • Targeting Lp(a) through interventions like apheresis shows promise for reducing cardiovascular events in high-risk individuals.