How to Survive the Zombie Apocalypse: What is Cellular Senescence

Skin Biology

Feb 22

What are Zombie Cells

All cells reach a point where they can no longer divide. Most of the time this leads to the cell dying. But not all cells do as they should. Some stop dividing but don’t die. They move around our body like zombies; alive just enough to spew out compounds that can “infect” surrounding cells and cause destruction of our skin’s architecture.

(This process is called cellular senescence and produces senescent cells- but hey we like the name zombie cells better).

As scary as they sound, zombie cells do serve a purpose within our bodies. They have been shown to help with tissue repair and even act as a barrier for potential tumor growth.

On the flip side, cellular senescence has been identified as one of the hallmarks of aging. So, it makes sense that these zombies have been a key area of research in the field of pharmaceutical and cosmetic science.

Once a cell becomes a zombie, they begin releasing an irritating brew of inflammatory molecules (ex. cytokines) with the goal of triggering our body's immune system to know to come and find them for removal. When we are young our immune system is pretty good at hunting down these zombies and getting rid of them. But as we age our immune system can’t fight them off quite as well leading to, well, a zombie apocalypse of sorts [1,2].

This army of zombies now has the power to damage surrounding areas with its unique secretion of inflammatory compounds, sometimes even leading to the creation of new zombie cells. And because these cells can’t divide it reduces the number of healthy cells within our skin, threatening our skin’s overall efficiency. This accelerates those pesky signs of aging like wrinkles and sagging.

How Zombie Cells Form

Simply put, senescent cells are the result of damage. This damage can be from natural changes that happen as we age or from external sources like the sun. The formation of zombie cells is complex but is generally believed to be largely controlled by the activation of either the p53-p21 and/or p16 pathways. If either pathway becomes overexpressed due to various stressors, cellular senescence can occur [1,2].

It is estimated that our DNA undergoes damaging events between 10,000-100,000 times a day! [9] To combat these possible threats, our cells have a system for scanning and trying to fix damage within our DNA, called the DNA damage response (DDR). This response team scans our DNA and places flags in spots where damage has occurred. This flagging system alerts our cells’ repair men to come fix the problem. But as we age, these flags grow in number which causes an overactive DDR [9]. If the repair men can’t keep up, this can trigger the activation of the pathways mentioned above. This activation can affect the regulation of the cell-cycle, stopping it from dividing, turning it into a zombie.

And it’s not like this damage is going anywhere as we get older. The prolonged activation of the DDR changes the cell's behavior, telling it to increase the production of that inflammatory brew. It really becomes a vicious cycle of constant triggering of DNA repair which increases zombie cells and the inflammatory molecules they release which then can cause further damage and more zombie cells.

It is a complex process that has a multitude of possible causes, making it hard to prevent their formation in the first place. And once it gets going, it is even harder to stop.

How to Survive the Zombie Apocalypse

While the process is complicated and not fully understood, we do have a few weapons in our arsenal for surviving this zombie apocalypse.

Reduce UV Induced DNA Damage and Reactive Oxygen Species (ROS)

First things first is protecting the skin from the sun. This is the first step in preventing damage to our DNA and the formation of reactive oxygen species.

If we reduce damage and ROS we reduce the likelihood of triggering cellular senescence.

What is the easiest way to protect the skin from the sun? You guessed it- sunscreen!

But let’s be real, most of us suck at wearing sunscreen (or remembering to reapply it). Reactive oxygen species are bound to form which can overwhelm our skin’s internal antioxidant system. That is where topical antioxidants come in handy, rendering these molecules harmless before they can do any real damage.

Help our DNA Repair Itself

Like we mentioned above, if the DDR can’t keep up it can send the cell down the path of self-destruction. If we can boost our skin's natural repair mechanisms, we may just be able to keep all those repair flags down to an acceptable level.

One ingredient that has gotten some spotlight recently among consumers for its cell repairing capability is Ectoin, but there are other ingredients on the market that have this capability.

If severe damage occurs, little fragments of DNA may seep out into the cell where they don’t belong. Helping our cells’ garbage men clean up the mess can keep the overall inflammatory response down. Try looking for ingredients that boost our skin’s autophagy process.

Improve Mitochondrial Function

We all remember one thing from high school biology and that is that the mitochondria are the powerhouse of the cell. When this energy producer isn’t functioning right it can also release ROS (see above). But we also might see issues with forming NAD+ which can lead to low ATP (energy) and activate the pathway to senescence.

One way our skin produces NAD+ is through the conversion of Vitamin B3. (Giving your skin a topical boost of niacinamide isn’t such a bad idea).

In order to get from B3 to NAD+ the enzyme NAMPT is necessary. Ensuring we have enough of this enzyme ensures this critical step occurs.

(Peep RejuveNAD™ by Mibelle that has data for boosting NAMPT production).

Another ingredient that has been long recognized for its anti-aging benefits is CoQ10. The molecule helps to transport electrons in the mitochondrial respiratory chain (which is the process for creating ATP). Keeping this energy production running effectively means the cell has less of a chance of becoming a zombie.

Maintain Telomere Length

At the end of our chromosomes are something called Telomeres. They basically act to maintain stability and prevent degradation of our precious DNA [3,4].

Every time our cells divide the telomeres shorten due to the fact that this sequence can’t be fully copied. The downside is that once they reach a certain length our cells' DNA damage repair (DDR) machinery is activated. Which we talked about above can lead to the creation of a zombie [3,4].

One clever way of preventing this shortening with each divide is through an enzyme called Telomerase. This enzyme helps to maintain Telomere length by re-adding some of the lost material [3,4].

But of course as we age the levels of Telomerase declines. So, what can we do? Apply an ingredient that helps to boost the expression of the Telomerase genes.

(Peep Lapagyl by Lipotec that has data for this).

With these zombie fighting strategies, hopefully you will become more armed for surviving the inevitable zombie apocalypse as we age.

Thanks for coming along for the zombie apocalypse. As always, I hope you gained a deeper understanding for the complexities of our skin. Stay inspired!