Cellular senescence

Well, so there are two ways that we can do that.

W- we know that part of what's happening that's causing this loss of hydration, it's, one is the accumulation of the senescent cells.

So as you have more senescent cells in your skin, you are gonna have less cells producing collagen, producing the, the structure that holds the water together.

You're gonna have more inflammation that is basically leading to protein, to enzymes, that will degrade collagen.

So you have collagen, you have hyaluronic acid, and so you are losing this, this system that's working well inside the skin.

It's all been compromised.

So the way that we're doing h- we're solving this problem is primarily with our peptide.

That is gonna help, like, reducing the amount of senescent cells, reduce the inflammation, and we created the peptide in a formula that's now supporting collagen production, is supporting elastin production, hyaluronic acid production.

It's a killer.

I wanna, I wanna transition into senescent cells, right? And some people call them zombie cells because they have the ability to kinda, uh, infect other cells into this-

Yeah

... zombie-like status.

But now we're going to get directly into the basic research, like we did yesterday and I think the last two or three lectures.

So cellular senescence, something we've been discussing, because you know this is a primary fate of cells.

Physiological process with genetic determinants and epigenetic regulations.

That epigenetic regulation moves through external modification, which includes stress.

And Aging isn't something that only occurs in the advanced elderly.

It is a lifelong teleological biochemical process.

That includes specifics of cellular senescence, plus a very, very, very deep discussion of of how the terminus of the living system is relatively uncertain.

That is, how the living system will ultimately track to mortality and whether or not any of the aging processes will specifically contribute to not just the rate, but to the quality of the morbidity leading to death.

Next, I'd like to talk about a fascinating feature of aging involving cells that essentially retire, but don't leave.

These are called senescent cells.

A senescent cell remains alive, but permanently stops dividing.

This can happen because of DNA damage, telomere dysfunction, or other cellular threats.

And cellular senescence isn't inherently bad.

If a severely damaged cell is at risk of becoming cancerous, preventing that cell from continuing to divide can be protective.

Senescent cells can also play useful roles in processes such as wound healing.

The problem occurs when too many of these cells accumulate.

It was published in Nature Cell Biology.

The title is SARS-CoV-2 Infection Induces DNA Damage Through CHK1 Degradation and Impaired 53BP1 Recruitment and Cellular Senescence.

So this study found that there are three mechanisms through which the presence of the spike protein, in this case they're calling it a SARS-CoV-2 infection, interferes with DNA repair mechanisms.

Those three are, number one, ORF6 and NSP13.

That's one.

The second mechanism, N-protein, it competes with 5,3-BP1 for binding to damage-induced long non-coding RNAs, reducing 5,3-BP1 focal recruitment at the double-strand breaks.

Overall, what it's caused are impaired S-phase progression, DNA damage, inflammation, cellular senescence, which is cells going into a little coma, and premature aging.

So there's another study that supports all of this.

I want to be able to be functional, living happy, and excited about it.

That's my real key, and I think if we can slow down aging... or stop cellular aging and just chronologically age over time, we could do this, right? We've seen ourselves become a society of, we live in a 77, but really our health span is at 65.

We have 12 years of...

I mean, let's just be honest.

Instead, it enters a state called senescence.

You may have heard senescent cells described as zombie cells.

The cell is still alive but has stopped performing many of its normal functions.

Even more importantly, some senescent cells begin releasing signals like cytokines that can change what is happening in the surrounding tissue.

Researchers call this collection of signals a senescence-associated secretory phenotype, or SASP.

You do not need to remember the term.

What I want you to remember is that a damaged aging cell can remain in the tissue and release signals that promote inflammation and affect neighboring cells.

Imagine an employee who stops doing the job they were hired to do but continues showing up every day and sending disruptive messages throughout the company.

It remains metabolically active, but it's fundamentally broken.

And as you age, these senescent cells just begin to accumulate all over your body.

We find them building up in your skin, your kidneys, your blood vessels, muscle tissue, and even visceral fat.

OK, let's unpack this, because if they are just sitting there not dividing, you might logically think they're just, I don't know, taking up dead space.

But to understand the weapon, you first have to understand the zombie's armor.

Okay, lay it on me.

In these damaged senescent cells, there is a very specific survival mechanism that's keeping them alive against all odds.

There is a protein called FOXO4.