Health and Healthcare Systems

These genes could be the key to longer lifespans

An old couple sitting on a bench looking at a mountain range

Species that live longer tend to have low expression of genes involved in energy metabolism and inflammation. Image: Unsplash/Matt Bennett

Lindsey Valich
Writer, Futurity
Share:
Our Impact
What's the World Economic Forum doing to accelerate action on Health and Healthcare Systems?
The Big Picture
Explore and monitor how Ageing and Longevity is affecting economies, industries and global issues
A hand holding a looking glass by a lake
Crowdsource Innovation
Get involved with our crowdsourced digital platform to deliver impact at scale
Stay up to date:

Ageing and Longevity

  • Two regulatory systems controlling gene expression appear to be critical to the length of our lifespan, according to biologists at the University of Rochester.
  • Long-lived species tend to have low expression of genes involved in energy metabolism and inflammation, and high expression of genes involved in DNA repair and RNA transport.
  • Healthy sleep schedules and avoiding exposure to light at night could boost our lifespan by reducing the expression of genes involved in energy metabolism and inflammation.

Natural selection has produced mammals that age at dramatically different rates. Take, for example, naked mole rats and mice. The former can live up to 41 years, nearly ten times as long as similar-size rodents such as mice.

What accounts for longer lifespan? According to the new research from biologists at the University of Rochester, a key piece of the puzzle lies in the mechanisms that regulate gene expression.

In a paper in Cell Metabolism, the researchers investigated genes connected to lifespan. Their research uncovered specific characteristics of these genes and revealed that two regulatory systems controlling gene expression—circadian and pluripotency networks—are critical to longevity.

The findings have implications both in understanding how longevity evolves and in providing new targets to combat aging and age-related diseases.

Discover

What is the World Economic Forum doing to combat Alzheimer's?

The researchers compared the gene expression patterns of 26 mammalian species with diverse maximum lifespans, from two years (shrews) to 41 years (naked mole rats). They identified thousands of genes related to a species’ maximum lifespan that were either positively or negatively correlated with longevity.

They found that long-lived species tend to have low expression of genes involved in energy metabolism and inflammation; and high expression of genes involved in DNA repair, RNA transport, and organization of cellular skeleton (or microtubules).

Previous work from the researchers has shown that features such as more efficient DNA repair and a weaker inflammatory response are characteristic of mammals with long lifespans.

The opposite was true for short-lived species, which tended to have high expression of genes involved in energy metabolism and inflammation and low expression of genes involved in DNA repair, RNA transport, and microtubule organization.

When the researchers analyzed the mechanisms that regulate expression of these genes, they found two major systems at play. The negative lifespan genes—those involved in energy metabolism and inflammation—are controlled by circadian networks. That is, their expression is limited to a particular time of day, which may help limit the overall expression of the genes in long-lived species.

This means we can exercise at least some control over the negative lifespan genes.

“To live longer, we have to maintain healthy sleep schedules and avoid exposure to light at night as it may increase the expression of the negative lifespan genes,” says Vera Gorbunova, professor of biology and medicine at the University of Rochester.

Have you read?

On the other hand, positive lifespan genes—those involved in DNA repair, RNA transport, and microtubules—are controlled by what is called the pluripotency network. The pluripotency network is involved in reprogramming somatic cells—any cells that are not reproductive cells—into embryonic cells, which can more readily rejuvenate and regenerate, by repackaging DNA that becomes disorganized as we age.

“We discovered that evolution has activated the pluripotency network to achieve longer lifespan,” Gorbunova says.

The pluripotency network and its relationship to positive lifespan genes is therefore “an important finding for understanding how longevity evolves,” says Andrei Seluanov, professor of biology and medicine.

“Furthermore, it can pave the way for new antiaging interventions that activate the key positive lifespan genes,” Seluanov says. “We would expect that successful antiaging interventions would include increasing the expression of the positive lifespan genes and decreasing the expression of negative lifespan genes.”

Loading...
Don't miss any update on this topic

Create a free account and access your personalized content collection with our latest publications and analyses.

Sign up for free

License and Republishing

World Economic Forum articles may be republished in accordance with the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International Public License, and in accordance with our Terms of Use.

The views expressed in this article are those of the author alone and not the World Economic Forum.

Share:
World Economic Forum logo
Global Agenda

The Agenda Weekly

A weekly update of the most important issues driving the global agenda

Subscribe today

You can unsubscribe at any time using the link in our emails. For more details, review our privacy policy.

Funding the future: Sustainable financing models to help the fight against antimicrobial resistance

Shyam Bishen

October 10, 2024

About us

Engage with us

  • Sign in
  • Partner with us
  • Become a member
  • Sign up for our press releases
  • Subscribe to our newsletters
  • Contact us

Quick links

Language editions

Privacy Policy & Terms of Service

Sitemap

© 2024 World Economic Forum