Antiaging is a huge area. With our aging population (yes, I am in there), it is projected 2 billion people will be over the age of 65 in the year 2050. So how do we age well? How can we improve our cellular health to try to avoid chronic conditions?
What are we targeting?
- genomic instability
- telomere shortening
- epigenetic changes
- cellular senescence
- stem cell exhaustion
- loss of proteostatsis
- deregulated nutrient sensing
- mitochondrial dysfunction
- altered intercellular communication.
These are all looking at basic cell health. As your cells divide and regenerate, we need them to do so efficiently, effectively, and without errors. This helps ALL aspects of you- your cells are the basic building blocks of your skin, muscles, and every organ in your body.
The major focus of much of the current studies I am reading in my plastic surgery literature (this is in the October 2022 issue of Plastic and Reconstructive Surgery, “Cellular Senescence in Aging, Tissue Repair, and Regeneration”) are on senescence.
So let’s talk about cellular senescence.
Senescence is when the normal cell cycle is stopped by exposure to damage or stress. What are these triggers?
- oxidative stress (which can also hurt the mitochondria), increased reative oxygen species
- mechanical stress
- genotoxic stress
- telomere shortening
- mitochondrial dysfunction
- oncogene activation
As the DNA damage increases with age, genomic instability happens. The DNA repair machine can’t repair things well. This leads to cellular decline. When senescent cells happen, they release inflammatory factors. They are increased in number in things you have heard of: pulmonary fibrosis, osteoarthritis, inflammatory bowel, obesity, viral infections, liver cancer.
But they also seem to be temporarily released during tissue healing when healing from surgery, muscle regeneration, and organ regeneration.
There seem to be two types of senescent cells: DELETERIOUS and HELPER.
- Helper cells: promote stem cell function, wound healing, tissue regeneration
- Deleterious: promote chronic inflammation, impaired wound healing, aging
And there seems to be two cycles: temporary senescence and chronic.
So it isn’t totally straightforward.
Senescence is seen in facial and skin aging, acute wounds and delayed wound healing, chronic wounds, scarring, nerve repair and regeneration, and bone fracture healing.
It seems we may want to facilitate temporary senescence, as this leads to tissue repair, but inhibit the chronic senescence that leads to aging. We want to help the helper senescent cells and get rid of the deleterious ones.
How do we do that?
Welcome to the focus of antiaging. Senescence is a way to measure how quickly your cells are aging. So we can use that to help figure out what antiaging techniques are hype and which are real.
Stay tuned.