Saranya Wyles, M.D., Ph.D.

This is your active pigment production.

When you lose that ability, it actually contributes to dullness, to dispigmentation, to ineffective ways of combating UV protection.

So when this happens, you're losing both

functional ability for skin protection against UV damage and you lose structural change.

So you start to see dyspigmentation and a lot of my patients come in and say, all of a sudden I noticed this brown spot on my skin.

It's happened overnight.

All of a sudden I'm seeing this change.

So skin aging can feel like it happens overnight, but really it's years of molecular underlying biological damage that accumulates and it manifests as structural and functional change.

We look at the skin as a collective unit.

So think about it as epidermal aging, epidermal regeneration, and dermal aging and dermal regeneration.

So melanocytes live in the epidermis.

They're part of that milieu or microenvironment.

They interact with keratinocytes.

And then in the dermal aging, this is fibroblasts, macrophages, immune cells are also there.

So really, it's this collective home of epidermal and dermal aging that interface together.

And that influences how each player is activated.

So if you look at senescence, for example, senescence is this

that can happen with aging.

These are zombie cells or cell cycle arrest that happens over time.

So when a fibroblast or melanocytes undergoes senescent cell cycle arrest, it influences that entire skin homeostasis.