This 'selfish' gene may prevent heart disease

The gene, called MeXis, acts within key cells inside clogged arteries to help remove excess cholesterol from blood vessels.

Published: 14th February 2018 04:12 PM  |   Last Updated: 14th February 2018 04:12 PM   |  A+A-

Image used for representational purpose

By IANS

NEW YORK: Scientists have identified a "selfish" gene that can potentially remove cholesterol from blood vessels and help prevent heart disease.

The gene, called MeXis, acts within key cells inside clogged arteries to help remove excess cholesterol from blood vessels.

In mice, MeXis was found to control the expression of a protein that pumps cholesterol out of cells in the artery wall, said researchers from the University of California-Los Angeles (UCLA).

In the study, published in the journal Nature Medicine, researchers found that mice lacking MeXis had almost twice as many blockages in their blood vessels compared to mice with normal MeXis levels. 

In addition, boosting MeXis levels made cells more effective at removing excess cholesterol.

MeXis is an example of a "selfish" gene, one that is presumed to have no function because it does not make a protein product. 

However, new studies have suggested that these so-called "unhelpful" genes can actually perform important biological functions without making proteins and also produce a special class of molecules called long non-coding RNAs, or lncRNAs.

"The idea that lncRNAs are directly involved in very common ailments such as plaque build-up within arteries offers new ways of thinking about how to treat and diagnose heart disease," said lead author Tamer Sallam, Assistant Professor at the UCLA. 

"There is likely a good reason why genes that make RNAs rather than proteins exist. A key question for us moving forward is how they may be involved in health and disease," Sallam added.

Considering many genes like MeXis have completely unknown functions, the study suggests that further exploring how other long non-coding RNAs act will lead to exciting insights into both normal physiology and disease, the researchers said.
 

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