Interfering RNA to Reduce Lipoprotein(a) in Cardiovascular Disease

 

Cardiovascular disease is the leading cause of death and disability worldwide. Lipoprotein(a) is a low-density lipoprotein variant containing a protein called apolipoprotein(a). High levels of lipoprotein(a) are a causal risk factor for atherosclerotic cardiovascular disease. It also influences inflammatory processes as well as the function of leukocytes, and vascular and cardiac cells, thereby impacting vessels and the heart. Statins form the select therapy with the aim to block cholesterol synthesis, although additional lipid-lowering drugs are required to achieve low-density lipoprotein cholesterol target values. 

A recent study has discovered that olpasiran therapy significantly reduces lipoprotein(a) concentrations in patients with atherosclerotic cardiovascular disease. Olpasiran is a small interfering RNA that reduces lipoprotein synthesis in the liver. The study conducted a randomized, double-blind, placebo-controlled, dose-finding trial in which patients with atherosclerotic cardiovascular disease and lipoprotein(a) concentration of more than 150 nmol per liter were involved. Patients were randomly assigned to receive one of four doses of olpasiran or a matching placebo. After nine months, the lipoprotein concentration had increased by a mean of 3.6% in the placebo group while olpasiran therapy had substantially and significantly reduced the lipoprotein(a) concentration in a dose-dependent manner. 

With cardiovascular disease being the leading cause of mortality and morbidity worldwide, effective and worthwhile therapies to reduce cardiovascular risk are highly needed. In so, I believe that further trials are required to determine olpasiran therapy's effect on cardiovascular disease, not just atherosclerotic cardiovascular disease.  Although from the previous trial on atherosclerotic cardiovascular disease, olpasiran therapy seems to be a promising therapy for individuals with high lipoprotein(a) levels who currently don't have any effective therapies to lower their concentration. 

The Cause of Chewy Chicken Meat!

The Cause of Chewy Chicken Meat!

Almost everyone eats chickens, and ever wonder why some chicken meat is soft and some hard and chewy? Recently published, the University of Delaware researchers have discovered that lipoprotein lipase in chicken may contribute to wooden breast syndrome. Lipoprotein lipase is an enzyme that is important for fat metabolism. For decades, researchers have been studying wooden breast syndrome in broiler chickens that involved with analyzed genes in the disease and the identified biomarker for the disorder. The researchers also explain the hardened breast tissue from these chickens.

How did these researchers find that lipoprotein lipase is the answer? The researchers know that breast muscle fibers in chicken reply on sugar, which is a glucose molecule for fuel and not fat molecules in this case. They use RNA sequencing to determine which genes expressed, and finally, they found evidence of lipoprotein lipase expressed in endothelial cells. Since fat oxidized for energy in the breast, it causes another excess release of the free radical molecule that modifies the terrible fats and protein, which then causes a problem for the chicken’s immune system. This eventually leads to hard and chewy chickens.


This is a useful finding that researchers were able to discover. This would help growers manage to be more cautious about what they feed or look over how the conditions of the chicken are before actually going into the market, processed for meat, or breeds that may result in economic losses or disease spreading.


https://www.sciencedaily.com/releases/2019/11/191120175613.htm
https://eurekalert.org/pub_releases/2019-11/uod-tco112019.php

Favorable CETP Variant Can Signify A Longer Life

        A new study found that people with a particular gene variant, in the gene CETP, may survive the longest. CETP, cholesteryl ester transfer protein, is located on chromosome 16. It is a plasma protein that facilitates the transfer of cholesteryl ester from high density lipoprotein (HDL) to other lipoproteins. HDL is known as the "good" kind of cholesterol, and an increase in the blood levels of HDL is caused by the favorable variant of the CETP gene.  

        For a long time, researchers knew that people with this gene variant have a better chance at living longer than 95, and sometimes even 100, years. A new study, presented by Dr. Sofiya Milman, shows that when comparing elderly people above the age of 95, the people with the advantageous variant of the CETP gene outlive the other elderly people. This study expands on the work began at Einstein College of Medicine in New York City in the 1990s. When describing the centenarians she has studied, Milman says, "They don't only live longer, they live healthier too."
        Before conducting the study Milman was aware that the CETP variant was found to be related to decreased rates of heart disease and strokes and sharper mental function. Milman conducted the study by gathering 400 ninety-seven year old New York residents and following them for about one to eleven years. The researchers found evidence confirming that people with the favorable CETP variant and higher HDL levels lived longer.

 

        CETP and HDL are not the only keys to a long life. Exercise, healthy eating, and adequate sleep are still some very important aspects to a long and healthy life. Understanding CETP, HDL, and other "longevity" genes are still important and may open many doors in the research world. "Down the road, it might be possible to develop therapies that mimic these genes' effects," Milman believes.

        This article stood out to me because the subject of long life is really interesting to me. As a child, I always believed that researchers would eventually invent a "magic potion" that caused everybody to live forever. Hearing there is a gene that effects one's life span and that drug companies have already started working on CETP inhibitors, makes my childhood assumption sound closer than ever. Now that I think about everybody living forever, it might not actually be a good thing. Overpopulation would be an extreme concern and resources would diminish even quicker. This article is still very fascinating and makes me wonder if I could possibly have the favorable CETP variant.

Main Article:  http://medicalxpress.com/news/2014-11-longevity-gene-key-life.html
Related Article: http://www.sciencedaily.com/releases/2010/01/100112165234.htm

Genetic Cause Found for Clogged Arteries

It is believed that blood pressure and cholesterol levels are not the most accurate way of assessing the risk of heart attack and stroke. Instead, it is now said that measuring calcium build-up in the arteries gives a better indicator of the likelihood of heart problems. Calcium build-up in the arteries marks the calcification of plaque, which results in hardening that can lead to heart attacks. Recently, it has been found that a genetic variation increases one’s risk of developing these deposits in the heart. This variation gives us essential clues as to how we should treat the disease that is found in nearly 7% of the world’s population. Wendy Post, from the Johns Hopkins University School of Medicine said “The latest findings could lead to the development of targeted medications to slow the progression of the disease, which can cause chest pain and shortness of breath, and can in some cases require surgery”.

 The gene that is currently being looked at is involved in the production of lipoprotein, a type of cholesterol particle that circulates in the blood. It has been said that high levels of lipoproteins are connected aortic valve disease. But, in previous years, scientists were not able to determine if it was just a marker of the disease or a casual factor. “Our results provide the first evidence for a casual relationship,” exclaimed Wendy. After surveying around 7,000 people, and looking at 2.5 million gene variants, it was found that the particular variant was strongly associated with the aortic calcium deposits.

When looking around for articles this one particularly caught my eye because a few years ago my dad found out that he had severely clogged arteries. After reading through this article, it was interesting to learn that a genetic variation could have likely been the cause for his blockage. With these new findings that there is the possibility for developing medications to target and slow the progression of the calcium deposits. It’s exciting that these findings have the potential to go on and affect the future of diagnosing and treating aortic valve disease.

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