Cell Senescence & Vascular Disease

Your left arm begins to hurt just a bit. Throbbing, the pain rapidly gets worse. Suddenly, your heart stops. You feel faint, and you collapse.

Sound familiar? I just described a heart attack. Every 40 seconds, someone in the USA has one. That’s insane.

48.5 percent of Americans deal with heart disease day by day. And today I’m going to tell you why.

A little bit more about vascular disease

Vascular disease can be defined as any condition of the blood vessels.

Some examples are heart attacks and atherosclerosis.

There are many risk factors and phenotypes of these diseases, but there is 1 culprit behind these.

And the culprit is…

drumroll please……

CELL SENESCENCE!

Bet you weren’t expecting that foreign word (or maybe you were, it’s in the title). Let me explain.

The basics of cell senescence

Cellular senescence is a cell state reached once cells have divided a finite amount of times. This occurs in normal human somatic cells.

This occurs when our cells divide. When cell division occurs, we copy the DNA from the ends of our chromosomes. Unfortunately, this process isn’t perfect, and a little bit of DNA is cut off at the ends.

We don’t want to lose all this valuable DNA information, so our bodies have these things called telomeres. They’re like the aglets on the ends of our shoelaces (plastic things), and they’re bits of dispensible DNA information on the ends of our shoelaces.

After a while, our cells stop dividing because our telomeres have gotten too short. This happens after around 50–70 divisions, the Hayflick limit.

Other than telomere shortening/attrition, several factors can induce cellular senescence.

• One is oxidative stress. This is essentially a buildup of free radicals, which are molecules missing an electron.
• Another is mitogenic and oncogenic signaling. When oncogenes (cancer genes) signal, this additionally induces senescence!

Now, how are these linked?

The Link

This talks about the various characteristics of CVD, (e.g. how the disease in different groups of people can be driven by different genes and speed).

Cellular senescence can cause different phenotypes downstream, such as plaques, caused by lipid-filled macrophages, which cause the disease atherosclerosis.

However, if the cells’ proteins cause blood clots, and arteries are blocked, this might cause a coronary infarction .

Cellular senescence has a lot of links to these phenotypes.

Cellular senescence can also be driven by risk factors such as hypertension, which induces it.

So… how do we prevent this?

Cell Senescence Treatments

There are a few treatments for senescence.

1. Telomerase — This is an enzyme that extends the telomeres in our cells, and the higher its activity, the more cells can divide. Companies like Telocyte are working to integrate this as a therapy for senescence.
2. Senolytics — Drugs used to selectively eliminate senescent cells. Accuracy is being improved right now, and my own company, Biotein, is working on this!
3. Natural processes — Processes like autophagy, which recycle damaged cell parts and remove senescent cells can also be useful. This can be initiated with exercise and intermittent fasting.

Key Takeaways

• Vascular disease can be defined as any condition of the blood vessels.
• Cellular senescence is a cell state reached once cells have divided a finite amount of times.
• Cellular senescence can cause different phenotypes downstream and also be driven by risk factors of heart disease.

Thank you for reading my article :). I hope you liked the tips and tricks I dropped. Sign up for my monthly newsletter. It updates you on my progress that month, articles I’ve made, videos I’ve created, and conferences I’ve attended/spoken at!

If you want to continue the discussion, email me at kheranina@gmail.com or connect with me on Linkedin! I’m going to publish a paper on this soon, with Michael Fossel. Stay tuned for that.