Science News
from research organizations

New research can improve heart health by focusing on gene variant

Date:
June 18, 2014
Source:
University of Copenhagen
Summary:
A particular gene variant lowers the risk of arteriosclerosis by 41 percent, making the variant an obvious target for future drugs for cardiovascular disease treatment, researchers have demonstrated for the first time. The results are based on data from nearly 76,000 subjects. The research is highly relevant as at least one pharmaceutical company has a drug in the pipeline which inhibits precisely apolipoprotein C3.
Share:
       
FULL STORY

Danish researchers from the University of Copenhagen and Rigshospitalet have shown that people with variation in a gene that inhibits a specific protein in the blood – the so-called apolipoprotein C3 – have a significantly lower level of normal blood lipids than people without this gene variation.
Credit: Image courtesy of University of Copenhagen

Danish researchers from the University of Copenhagen and Rigshospitalet have shown that people with variation in a gene that inhibits a specific protein in the blood -- the so-called apolipoprotein C3 -- have a significantly lower level of normal blood lipids than people without this gene variation. Furthermore, the same individuals also have a 41 per cent lower risk of arteriosclerosis.

The research is highly relevant as at least one pharmaceutical company has a drug in the pipeline which inhibits precisely apolipoprotein C3, says Anne Tybjærg-Hansen, Chief Physician at Rigshospitalet and Clinical Professor at the Faculty of Health and Medical Sciences, University of Copenhagen.

The scientific results are based on two of the world's largest population studies, the Copenhagen City Heart Study and the Copenhagen General Population Study, with a total 75,725 participants who were followed for 34 years. The results have just been published in the New England Journal of Medicine.

By using genetic studies that mimic medical inhibition of apolipoprotein C3, we have demonstrated that the protein plays an important role in lowering the level of normal blood lipids and thus the risk of cardiovascular disease. People with lifelong hereditary inhibition of the protein have very low blood lipid levels (less than 1 mmol per litre of blood) as well as a significantly reduced risk of cardiovascular disease, says Anne Tybjærg-Hansen.

Need for better treatment

The primary objective of drugs which prevent cardiovascular disease is to lower blood cholesterol levels. But even among patients whose cholesterol levels are treated to target, there is still a residual cardiovascular risk. Triglycerides are lipids that are carried in the blood, the majority of which come from the food we eat. Triglycerides primarily serve as energy reserves for the body. However, high triglyceride levels in the blood, increase the risk of heart attack and arteriosclerosis.

Medical inhibition of proteins which increase the level of triglycerides is therefore an obvious target for new drugs, concludes Anne Tybjærg-Hansen.


Story Source:

The above post is reprinted from materials provided by University of Copenhagen. Note: Materials may be edited for content and length.


Journal Reference:

  1. Anders Berg Jørgensen, Ruth Frikke-Schmidt, Børge G. Nordestgaard, Anne Tybjærg-Hansen. Loss-of-Function Mutations inAPOC3and Risk of Ischemic Vascular Disease. New England Journal of Medicine, 2014; 140618140014007 DOI: 10.1056/NEJMoa1308027

Cite This Page:

University of Copenhagen. "New research can improve heart health by focusing on gene variant." ScienceDaily. ScienceDaily, 18 June 2014. <www.sciencedaily.com/releases/2014/06/140618184628.htm>.
University of Copenhagen. (2014, June 18). New research can improve heart health by focusing on gene variant. ScienceDaily. Retrieved June 30, 2015 from www.sciencedaily.com/releases/2014/06/140618184628.htm
University of Copenhagen. "New research can improve heart health by focusing on gene variant." ScienceDaily. www.sciencedaily.com/releases/2014/06/140618184628.htm (accessed June 30, 2015).

Share This Page: