Jove
Visualize
Contact Us

Related Concept Videos

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...
Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists01:18

Treatment for Pulmonary Arterial Hypertension: Endothelin Receptor Antagonists

Endothelins (ETs) are potent vasoactive peptides critical in the human body's various physiological and pathological processes. One of the most promising therapeutic strategies for treating pulmonary arterial hypertension (PAH) involves counteracting the effects of these endothelins using a class of drugs known as endothelin receptor antagonists.
ETs are synthesized through a complex sequence of enzymatic steps, primarily involving an enzyme referred to as endothelin-converting enzyme (ECE). Of...
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
Treatment for Pulmonary Arterial Hypertension: Oxygen Therapy for Respiratory Failure01:16

Treatment for Pulmonary Arterial Hypertension: Oxygen Therapy for Respiratory Failure

Oxygen therapy has emerged as a significant tool in enhancing the quality of life for patients suffering from pulmonary arterial hypertension (PAH). While this therapy has principally been studied on patients with significant hypoxemia, this therapeutic approach helps prevent potential organ damage and can be administered in the comfort of one's home.
Oxygen therapy is vital in increasing and maintaining blood oxygen levels in PAH patients. As a result, it aids in reducing fatigue, improving...
Chronic Pancreatitis II: Collaborative Care01:29

Chronic Pancreatitis II: Collaborative Care

The management of chronic pancreatitis is multifaceted, involving a comprehensive approach that includes thorough assessment, diagnostic testing, and a variety of management strategies.
Assessment:
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...

You might also read

Related Articles

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

Sort by
Same author

[New AHA and ACC guidelines on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk : Statement of the D•A•CH Society for Prevention of Cardiovascular Diseases, the Austrian Atherosclerosis Society and the Working Group on Lipids and Atherosclerosis (AGLA) of the Swiss Society for Cardiology].

Der Internist·2014
Same author

Fluorescence labeling and interaction of atherogenic lipoproteins with cultured cells.

Journal of fluorescence·2013
Same author

Transfer of pyrene-dietherphosphatidylcholine to serum lipoproteins.

Journal of fluorescence·2013
Same author

Expression of fat mobilizing genes in human epicardial adipose tissue.

Atherosclerosis·2011
Same author

Does lipoprotein(a) predict risk in type 2 diabetes?

European journal of clinical investigation·2006
Same author

Plasma delipidation process induces rapid regression of atherosclerosis and mobilisation of adipose tissue.

Journal of clinical apheresis·2005
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 Experiment Video

Updated: Jul 23, 2026

Rat Model of the Associating Liver Partition and Portal Vein Ligation for Staged Hepatectomy (ALPPS) Procedure
07:29

Rat Model of the Associating Liver Partition and Portal Vein Ligation for Staged Hepatectomy (ALPPS) Procedure

Published on: August 14, 2017

Therapy of hyper-Lp(a).

K M Kostner1, G M Kostner

  • 1Research Wing Level 3, Princess Alexandra Hospital, Woolloongabba, Queensland, Australia. KKostner@soms.pa.uq.edu.au

Handbook of Experimental Pharmacology
|April 7, 2006
PubMed
Summary

Elevated Lipoprotein (a) [Lp(a)] is a significant cardiovascular risk. Current treatments are ineffective, necessitating novel therapies targeting Lp(a) metabolism for hyper-Lp(a) patients.

Area of Science:

  • Cardiovascular Biology
  • Lipid Metabolism
  • Pharmacology

Background:

  • Lipoprotein (a) [Lp(a)] is a highly atherogenic lipoprotein, comprising an LDL core and apolipoprotein (a) [apo(a)].
  • Lp(a) levels are predominantly genetically determined (>90%) and influenced by apo(a) biosynthesis.
  • Impaired catabolism, as seen in kidney disease, can elevate Lp(a) levels significantly.

Purpose of the Study:

  • To review the current understanding of Lp(a) metabolism and its clinical implications.
  • To highlight the lack of effective treatments for elevated Lp(a).
  • To explore potential therapeutic strategies for hyper-Lp(a).

Main Methods:

  • Literature review of Lp(a) structure, genetics, metabolism, and therapeutic interventions.
  • Analysis of factors influencing Lp(a) levels, including genetic, hormonal, and disease-related aspects.

More Related Videos

Robotic Lateral Pancreaticojejunostomy for Chronic Pancreatitis
08:10

Robotic Lateral Pancreaticojejunostomy for Chronic Pancreatitis

Published on: December 14, 2019

Laparoscopic Left Lateral Sectionectomy: Guided by the Ligamentum Teres Hepatis and the Umbilical Fissure Vein
03:33

Laparoscopic Left Lateral Sectionectomy: Guided by the Ligamentum Teres Hepatis and the Umbilical Fissure Vein

Published on: September 27, 2024

Related Experiment Videos

Last Updated: Jul 23, 2026

Rat Model of the Associating Liver Partition and Portal Vein Ligation for Staged Hepatectomy (ALPPS) Procedure
07:29

Rat Model of the Associating Liver Partition and Portal Vein Ligation for Staged Hepatectomy (ALPPS) Procedure

Published on: August 14, 2017

Robotic Lateral Pancreaticojejunostomy for Chronic Pancreatitis
08:10

Robotic Lateral Pancreaticojejunostomy for Chronic Pancreatitis

Published on: December 14, 2019

Laparoscopic Left Lateral Sectionectomy: Guided by the Ligamentum Teres Hepatis and the Umbilical Fissure Vein
03:33

Laparoscopic Left Lateral Sectionectomy: Guided by the Ligamentum Teres Hepatis and the Umbilical Fissure Vein

Published on: September 27, 2024

  • Evaluation of the efficacy and limitations of existing lipid-lowering drugs on Lp(a).

    • Main Results:

    • Lp(a) size polymorphism is linked to kringle-4 Type-II repeats in apo(a).
    • Plasma Lp(a) levels correlate with apo(a) biosynthesis, with limited influence from diet or lifestyle.
    • Anabolic steroids are the only agents found to significantly reduce Lp(a), but are unsuitable for therapeutic use.

    Conclusions:

    • There is a critical need for specific medications targeting Lp(a) biosynthesis, assembly, or catabolism.
    • Further research into anabolic steroid mechanisms could lead to safer, targeted Lp(a) therapies.
    • Development of novel drugs is essential for managing hyper-Lp(a) and reducing cardiovascular risk.