Telomere: the shoelace tip at the ends of chromosomes
At the ends of our chromosomes, there are repeating DNA sequences; these structures are called telomeres. A telomere is like the plastic tip of a shoelace — it keeps the DNA intact, preventing the ends from sticking together or deteriorating. Each time a cell divides, a portion of its telomere shortens. When the telomere falls below a certain length, the cell can no longer divide — it enters a state called "replicative senescence."
This mechanism is nature's safety system: cells that can divide indefinitely become cancerous. Telomere shortening prevents cells from unlimited division. But the cost of this safety is a decrease in tissue regeneration capacity over time. When the telomeres of stem cells in the basal layer of the skin shorten, the skin's regeneration time lengthens (this period, which is 28 days in people in their 20s, increases to 40-50 days in people in their 50s).
Senescence: cells that don't work but don't die
When the telomere reaches a critical level or the cell sustains severe DNA damage, the cell chooses one of two paths: apoptosis (programmed death) or senescence (silent arrest). A senescent cell does not die; but it does not divide and loses its function. The problem is: these cells are not silent either. They emit a biochemical signal complex called SASP (Senescence-Associated Secretory Phenotype). These signals trigger inflammation, increase collagenase, and push neighboring cells into senescence.
In scientific literature, these cells are now called "zombie cells." Perhaps the most important driver of skin aging is the accumulation of these zombie cells. In young skin, the proportion of senescent cells is below 1%; at age 70, this rate can increase to 15-30%.
Attention:Chronic UV exposure is the single most powerful factor accelerating senescence in fibroblasts. Therefore, SPF is not just a stain prevention tool, but a cell life protection tool.
Senolytics: zombie hunters
Since 2011, a class of drugs called senolytics has been developed in the scientific world. Senolytics are molecules that selectively push senescent cells to death. In animal studies, the clearance of senescent cells has been associated with functional rejuvenation, improved organ function, and extended lifespan. In human clinical applications, senolytics are still in early stages; however, some herbal compounds (fisetin, quercetin) and drugs (dasatinib) show senolytic effects.
Topical senolytics have begun to be developed specifically for the skin. Pioneering studies in this area have been conducted with quercetin+fisetin combinations. I do not yet have a routine senolytic protocol in my clinic — the data has not reached sufficient maturity. However, this field seems poised to fundamentally change skin longevity practice in the next 5 years.
Cells in young skin
- Basal layer actively dividing (28-day turnover)
- High density of Collagen Type I
- Fibroblasts healthy, secreting well
- Senescent cell ratio below 1%
- Low SASP signal, minimal inflammation
Cells in aged skin
- Turnover extended to 45-60 days
- Collagen decreased, fragmented
- Fibroblasts with limited capacity
- Senescent cell ratio increased to 10-20%
- Chronic low-level inflammation due to SASP