Photoaging 101: Skin cell turnover and Cellular Senescence

Updated:  July 4, 2020

What is photoaging?

We’ve all heard the term photoaging, but what does that really mean? 

Our skin changes how it functions as we grow older, and that process can be accelerated by sun exposure (photoaging). 

Photoaging manifests itself in our physical appearance as fine lines, wrinkles, and uneven skin tone. 

Today, we’re going to take a look at how our skin changes due to both chronological aging and photoaging.

Sun exposure hastens the effects of chronological aging, so protecting your skin from the sun by using anti-oxidant rich skincare products, shade, and clothing is important.

We’re starting out with a quick anatomy lesson.  Then, we’ll talk about how cellular turnover rates change due to photo-exposure (and regular aging) and we'll also talk about something called cellular senescence.

Be sure to stay tuned for the next post in this series where we dive deeper into the sun's impact on our skin’s structure and function.

A brief skin anatomy lesson

Before we start talking about how our skin changes due to sun exposure, we need a basic understanding of both skin anatomy (how our skin is structured) and skin physiology (how our skin functions).

This information is technical, but my job is to describe it in plain English, and I hope you’ll stick with me.

Let’s start out with a basic cartoon showing the layers of the skin.  The epidermis is the outermost layer of our skin and the dermis lies below it.

basic layers of the skin, the epidermis, dermis and subcutaneous fat tissue.  Cartoon shows hair follicle and sebaceous gland origins.


Layers of the Epidermis

The epidermis itself is composed of several skin layers as shown in the illustration below.  One thing to note – the stratum lucidum is only present on the soles of our feet and the palms of our hands.

 layers of the epidermis - the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale

That outermost layer of the epidermis, the stratum corneum, is just layers of dead skin, but LIVING cells down in the epidermis' stratum basale layer constantly migrate up from the innermost layer of the epidermis to the outermost replenishing the stratum corneum as dead skin cells naturally slough away.

Cell Turnover Rate Slows

There’s some debate about how long it takes for a cell in the stratum basale to migrate to the stratum corneum. 

Part of the reason for this debate is that our epidermis varies in thickness in different parts of our bodies from about 0.04 mm thick on our eyelids (about half as thick as a strand of hair) to about 1.6 mm thick (about twice as thick as that strand of hair) on our palms and soles. 

For this reason, migration of epithelial cells in some parts of the body takes longer when compared with other parts, and migration times vary considerably based on which part of the body is used to evaluate the "turnover rate".

What is known is that this cellular migration rate or cellular turnover rate slows by approximately 30% to 50% from our 30s to our 80s (Reference 4), and this happens while the total thickness of all our epidermal layers DECREASES (mostly due to flattening of rete ridges, which we’ll talk about in the next post). 

Chronic sun exposure also slows down the cellular turnover cycle.

Cellular Senescence

As we age, our cells are more prone to enter a state of senescence where they no longer divide.  For skin cells, our chronological age AND the amount of time we've spent in the sun promote senescence.

Senescent cells no longer divide, and senescent cells also release different signaling molecules than when they were normal healthy cells. 

Signaling molecules are how the cells of our body communicate with one another, kind of like talking or texting with nearby cells. 

Here’s where I'll throw out a technical term.  Why?  Because you cannot search for senescence without coming across this acronym.  If you don’t care to get so technical, skip to the next non-italicized paragraph. 

SASP – senescence-associated secretory phenotype.  Just what the heck does that mean? 

Phenotype is a set of characteristics displayed by (or in this case a set of behaviors that) distinguish senescent cells from normal cell types. 

Senescent cells have the following differences when compared with normal skin cells:

  • Senescent cells express (or secrete) high levels of inflammatory signaling molecules
  • Senescent cells resist programmed cell death (apoptosis)
  • Senescent cells no longer divide

Whereas SASP means ALL three of those characteristics, we normally see the term SASP when talking solely about the signaling molecules that senescent cells produce and the term SASP environment when talking about the micro-environment around those senescent cells.

Normal Cell Life Cycle vs. Senescent Cells

You may have heard of the Hayflick limit, and even if you haven’t, you may remember from high school biology that we have extra sequences of DNA nucleotides (DNA base pairs).  These extra base pairs, known as telomeres, don't code for any of our genes but are really important for DNA replication, which is why they're tacked onto the DNA strands that code for our genes. 

Telomeres allow DNA replication to occur by giving room for the enzymes responsible for replicating our DNA to attach onto the DNA molecule. 

Telomeres are not part of the sequence necessary for gene coding, and every time a cell divides (or replicates), the telomere length gets shortened a little (this is due to how replication of the DNA strand occurs and I'll go into this in more detail after this illustration). 

how enzymes replicate DNA - the role of telomeres in DNA replication

DNA replication and why telomeres are important for this process.

Notice the big green blob in the figure above.  That's the enzyme responsible for replicating the DNA strand.  You'll see that enzyme is pretty large (quite a few base pairs long). 

Due to its size, when that enzyme attaches and detaches from the DNA strand, it can't start replicating at the very end of the strand because it just doesn't attach to the very end of the strand, it inserts itself as close as possible at the end of the DNA strand, but there are base pairs that don't replicate during the process.

That's why telomeres are SO important. 

Telomeres reside at the end of our DNA strands adding length onto the DNA strand, and each time a cell divides and our DNA gets copied as part of that process, the telomere length gets a little shorter.

After a certain number of divisions, these telomere lengths are too short to allow the cell to continue dividing so that the full DNA sequence gets copied, so replication (and cell division) stops. 

The natural order of things is that this cell would destroy itself through programmed cell death (apoptosis).  However, it's also possible that these cells enter a state of senescence.  And, senescent cells resist programmed cell death. 

The choice of a path towards programmed cell death or senescence presents for all cells at the end of their division life cycle in all the tissues of our body. 

Senescence isn't a phenomenon unique to skin cells, but of course photo-aging is unique to skin cells.

Senescent skin cells tend to build up both in chronically photo-exposed skin and also naturally as we age (even in non-photoexposed skin).

Cascade effect of senescence

Remember we mentioned earlier that once a cell stops dividing (becomes senescent) that it starts producing different signaling molecules than it did when it was a normal cell? 

Some of those signaling molecules produced tell nearby cells to stop dividing also. 

So, a single non-dividing senescent cell can start a cascade or domino effect because it constantly tells nearby cells to stop dividing and they listen

This is how one senescent cell can demoralize its neighboring cells and turn the once happy, joyful, viable neighboring cells into other demoralized cells like itself spreading the message to stop dividing to their neighbors and propagating the whole process.

How to encourage removal of senescent skin cells

Researchers  have linked certain genes to higher rates of senescent cell removal (yep, good genes help) and have shown that certain supplements and ingredients boost the elimination of senescent cells.

When we’re talking about senescent skin cells in particular, we’re in luck because some ingredients have been shown to reduce the number of senescent skin cells or reduce the expression of the demoralizing signaling molecules that the senescent cells release.

Here’s a short list of ingredients shown to help reverse the effects of senescence in skin cells (we're just talking about skin on this list even though some of these ingredients have been shown helpful for reversing senescence in other cells within our body). 

Disclaimer:  Please keep in mind that these studies have not been evaluated by the FDA.

You can either add Vitamin C to your diet or apply it topically (both ways have been studied for reducing the number of senescent cells).

Goldenrod isn't nearly as common in skincare, but JuvelevenTM, an incredible peptide, is often found in skincare products because of its ability to protect skin from the effects of UV.

If you're interested in picking up a great serum with JuvelevenTM, we offer the peptide packed oil free Abigail's Serum, and you can find it here.

And, be sure to stay tuned for our next post on more ways sun exposure impacts our skin.

You can sign up for our newsletter so you never miss an article.


Reference 1 Basic Skin Layers

Reference 2 Wikipedia:  Epidermis

Reference 3 The Skin

Reference 4 A review: Effects of aging on skin structure and function

Reference 5

Reference 6 Goldenrod extract has a mild senolytic effect in a cell culture study

Reference 7

Reference 8

Reference 9 Greentech active ingredient promotes positive ageing

Reference 10

Additional references:


Brandy Searcy founder Rain Organica

About the Author

Brandy's a formulation scientist and self-proclaimed health geek who loves hiking, gardening, bird-watching, and body boarding. 

Her struggle with acne during her teens and 20s led to a holistic and healthy approach to skincare, embracing skin as an organ to be loved and cared for rather than a canvas to wage war on. 

Since 2008, she's been developing all-in-one products for a simple routine at home, & Rain Organica started when her backpacking friends asked for a portable skincare routine to keep their skin healthy & happy on and off the trails.

You can try Rain Organica for yourself with The Essentials Kit, a complete skincare routine in just 3 steps.

Brandy's LinkedIn Bio

Subscribe to our newsletter:

← Older Post Newer Post →

← Back to All Articles