Reports of a 'wrinkle cure' look a little saggy

Behind the Headlines

Monday January 9 2017

The research does offer the possibility of repairing scar tissue

As skin ages it loses its elasticity, leading to wrinkles

"Wrinkles could be a thing of the past as scientists find a way to regenerate fatty cells," The Daily Telegraph reports.

Research involving mice suggests a protein called bone morphogenetic protein (BMP) could repair skin damaged by scarring or ageing by stimulating the production of fat cells (adipocytes).

The research team wanted to investigate why mice that experience skin damage are able to produce new fat cells during the healing process. The same is not true for humans where injury results in some degree of scarring.

Human skin also loses its elasticity over time – leading to wrinkles – due to the gradual loss of adipocytes.

The researchers found the answer appears to lie in hair follicles. When the mouse wounds heal they produce new hair follicles (tiny sacs in the surface of the skin that anchor individual hairs). This in turn triggers the production of BMP which appears to cause damaged skin tissue to be "reprogrammed" into fat cells.

The researchers hope their findings may be used to develop new treatments to treat scar tissue in humans, and possibly (and likely much more profitably) reverse the signs of ageing.

But exactly how you safely replicate biological processes innate to rodents in humans is just one of the many wrinkles that will need to be ironed out before we can realistically start talking about an "elixir of youth".


Where did the story come from?

The study was carried out by researchers from University of Pennsylvania, University of California–Irvine, and various other institutions in the US and Europe. Funding was provided by the National Institutes of Health and the Edward and Fannie Gray Hall Center for Human Appearance, with individual researchers receiving grant support from several other sources.

The study was published in the peer reviewed scientific journal, Science.

The UK media over-hyped the implications of a very early-stage, lab based piece of research that involved no humans. Also, the fact that the work could possibly lead to an effective treatment for scarring was largely overlooked in favour of the potential for anti-ageing products.

However, it would appear that much of this hype was generated by the lead author of the study, Professor George Cotsarelis, who is widely quoted as saying: "Our findings can potentially move us toward a new strategy to regenerate adipocytes in wrinkled skin, which could lead us to brand new anti-ageing treatments."


What kind of research was this?

This was a laboratory study observing how wounds in mouse skin heal.

When wounds heal in humans they produce a scar with excess collagen but lacking in hair follicles and fat. Recent studies in mice have found that when wounds heal in mice they regenerate hair follicles which have fat cells (adipocytes) surrounding them. The adipocytes prevent scar wounds appearing in mice.

This study aimed to look into the repair mechanisms more closely and look at the cellular origin of the new fat cells. In particular they wanted to see if hair follicles were necessary for fat cells to form.


What did the researchers do?

The study involved conducting tests on mouse scar tissue in the laboratory. They cultured skin cells isolated from wounds to observe how they changed in the days and weeks following injury, looking at when the first new hair follicles appeared and when new fat cells appeared.

The researchers then looked into the cellular origins of the new fat cells and the processes that led to their development. They followed up their findings by looking at human scar tissue.


What did they find?

The researchers found that hair follicles seem to be necessary for new fat cells to form.

In mouse wounds new hair follicles started to form around 15 to 17 days after injury, followed by the first new fat cells at around 23 days, which then gradually increased in number.

In scar tissue with hair follicles many fat cells were seen, whereas none were seen in hairless scars.

Looking into the cellular origins of the fat cells, they seem to originate from myofibroblast cells – a cell type somewhere inbetween two cell types – fibroblasts, which are found in scar tissue, and smooth muscles cells. Therefore the origin of the fat cells was from a non-fat cell source.

New hair follicles seem essential to this myofibroblast reprogramming. New hair follicle formation triggers the release of the bone morphogenetic protein (BMP) which "kickstarts" the myofibroblast reprogramming. They demonstrated this process by using chemicals to block BMP signalling and found that fat cells did not form.

In their further laboratory tests in human scar tissue the researchers demonstrated they could form fat cells in the tissue in two ways: if they either treated the scar tissue (fibroblasts) with BMP, or alternatively cultured them with hair follicles. 


What did the researchers conclude?

The researchers conclude: "We identify the myofibroblast as a plastic cell type that may be manipulated to treat scars in humans."



This laboratory study furthers understanding of how wounds heal. It found that mouse skin wounds are able to regenerate new fat cells through signalling pathways triggered when new hair follicles form.

The researchers hope their findings may be developed and offer potential new ways to treat scar tissue in humans, enabling them to produce new fat cells that are normally lacking in a scar formed of connective tissue cells – hopefully ultimately improving the appearance of scars and making them look like normal skin.

And, as the media seized upon, there may be the possibility of repairing the effects of ageing on the skin.

However, a great deal more study would be needed to develop these findings, and see if they could be applied in the real world, rather than in the laboratory.


Analysis by Bazian

Edited by NHS Choices


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Scars: skin camouflage


Media last reviewed: 19/07/2015

Next review due: 19/07/2017