Beauty has traditionally focused on what we can see: hydration, texture, pigmentation, fine lines, and changes in firmness. But researchers investigating how skin changes over time are increasingly looking much further beneath the surface.
One area attracting attention is cellular energy.
Every skin cell needs energy to maintain its normal functions. Much of that energy comes from mitochondria, structures inside cells that help convert nutrients into adenosine triphosphate, better known as ATP. ATP provides readily usable chemical energy for countless cellular processes.
Mitochondria are therefore relevant to everything from basic cell maintenance to responses to environmental stress. Research into skin aging has also identified measurable differences in mitochondrial function between younger and older skin cells.
That does not mean mitochondria hold a simple key to younger-looking skin. It does, however, explain why cellular energy has become such an interesting area of beauty science.
What Does Cellular Energy Actually Mean?
“Cellular energy” sounds like the kind of phrase that could appear on the side of a serum bottle without much explanation. In biology, though, it has a specific meaning.
Mitochondria contain machinery involved in oxidative phosphorylation, a process through which cells generate much of their ATP. Researchers can investigate this system by measuring factors such as oxygen consumption, mitochondrial membrane potential, and spare respiratory capacity, the additional ability a cell has to generate energy when demand increases.
A 2020 Aging Cell study examined gene expression and mitochondrial function in human skin. Researchers found age-associated changes in genes involved in the mitochondrial electron transport chain and observed lower oxidative phosphorylation, mitochondrial membrane potential, and spare respiratory capacity in fibroblasts from older donors compared with younger cells.
The researchers described oxidative phosphorylation as the “top canonical pathway associated with aging in the face.”
Fibroblasts are particularly interesting in beauty research because they are connective-tissue cells involved in producing components of the extracellular matrix, including collagen.
When Mitochondria Become Messengers
The familiar description of mitochondria as the “powerhouses of the cell” is useful, but incomplete.
Scientists now know that mitochondria also participate in communication inside cells. One particularly intriguing area of research involves mitochondrial-derived peptides: small peptides associated with genetic information contained within mitochondria.
MOTS-c is one example. Researchers first reported the 16-amino-acid peptide in Cell Metabolism in 2015 after identifying a short open reading frame within mitochondrial 12S ribosomal RNA. The study investigated MOTS-c primarily in the context of cellular and metabolic regulation.
Research published in 2018 added another layer to the story. Under certain experimental conditions involving metabolic stress, researchers observed MOTS-c moving into the nucleus of cells, where it influenced nuclear gene expression through an AMPK-dependent process. AMPK is an enzyme involved in sensing cellular energy status.
For readers following this emerging field can visit licensedpeptides.com for more information, specifications and analytical information on MOTS-c as a research-use-only material.
The science is interesting because it changes the way we think about mitochondria. They are not simply factories producing ATP. Experimental research suggests that mitochondrial signals can also participate in the way cells respond to changing metabolic conditions.
Importantly, research into MOTS-c should not be confused with evidence for a cosmetic or beauty application. Its inclusion in this scientific conversation is about understanding mitochondrial communication, not establishing it as a skincare ingredient.
What Happens to Mitochondria as Skin Ages?
Several studies have examined whether mitochondrial characteristics differ with age.
A 2023 study published in Experimental Dermatology analysed human skin obtained from 21 younger and 22 older donors. Researchers looked at proteins involved in the mitochondrial electron transport chain as well as markers associated with mitochondrial mass and DNA transcription.
They found significantly lower levels of ATP5F1A, a component of complex V, and TFAM, a protein involved in mitochondrial DNA regulation, in the epidermis of older participants. The observed differences were independent of UV exposure in the particular skin sections studied.
Again, that does not mean mitochondrial changes alone explain visible ageing.
Skin ageing involves a complicated mixture of intrinsic biology and external factors, including ultraviolet radiation. Genetics, cellular signalling, structural proteins and accumulated environmental exposure all contribute to the picture.
Mitochondrial biology is one piece of a much larger puzzle.
Sunlight Adds Another Piece to the Puzzle
UV radiation provides a particularly useful example of how environmental exposure and mitochondrial biology can intersect.
In a study involving 52 people, previously unirradiated areas of skin were repeatedly exposed to physiologically relevant doses of UVA radiation. After two weeks, researchers found an approximately 40% increase in levels of a mitochondrial DNA mutation called the “common deletion.” Most of the detected increase occurred in the dermis.
Laboratory studies have also explored possible connections between UVA exposure, mitochondrial function and the formation of structural fibres.
A 2022 study using normal human dermal fibroblasts found that UVA exposure was associated with decreased intracellular ATP and poorer formation of type I collagen and fibrillin-1 fibres. Experimentally disrupting a protein involved in mitochondrial quality also reduced ATP and interfered with fibre formation.
These experiments help scientists explore mechanisms, but cultured cells are not the same as intact human skin. Mechanistic evidence should not automatically be translated into claims that changing mitochondrial activity will produce a particular visible result.
That distinction becomes especially important when scientific vocabulary enters beauty marketing.
What Niacinamide Can Teach Us About Beauty Science
There is already a familiar skincare ingredient that provides an interesting bridge between beauty and cellular metabolism: niacinamide.
Niacinamide, also known as nicotinamide, is a form of vitamin B3. It is involved in cellular pathways associated with nicotinamide adenine dinucleotide, or NAD+, an important molecule in energy metabolism.
In the 2020 Aging Cell study, researchers treated fibroblasts from older donors with nicotinamide under laboratory conditions. They reported changes in several mitochondrial measurements, including oxidative phosphorylation, mitochondrial number and membrane potential.
The study is a useful illustration of both the possibilities and limitations of mechanistic beauty research.
Showing that an ingredient affects isolated fibroblasts does not automatically tell us what a finished cosmetic will do to someone’s skin. Concentration, formulation, delivery, stability and clinical testing all matter.
In other words, an interesting mechanism is the beginning of the scientific story, not necessarily the end of it.
How to Read the Next Cellular Energy Claim
As beauty becomes more comfortable borrowing language from molecular biology, phrases such as “cellular energy,” “mitochondrial function,” and “cellular longevity” are likely to become more common.
A study showing that a molecule influences an intracellular pathway can be scientifically important without demonstrating that a product containing, or merely referencing, that molecule will change the appearance of skin.
Good beauty science should be interesting enough without needing to blur that distinction.
Conclusion
The growing conversation around cellular energy reflects a wider change in beauty science. Researchers can now investigate skin not simply as a surface but as a living system shaped by metabolism, environmental exposure, and communication between cells and their internal structures.
Research into mitochondrial function, ATP production, UV exposure, and mitochondrial-derived peptides is helping scientists understand cellular biology in increasingly fine detail. It is also giving beauty readers a new scientific vocabulary to navigate.
But perhaps the most useful takeaway is also the simplest: fascinating biology is not the same thing as a proven beauty benefit.
Looking beyond the glow means appreciating both sides of the story—the excitement of emerging science and the importance of asking what the evidence actually demonstrates.
References
Berneburg, M., Plettenberg, H., Medve-König, K., Pfahlberg, A., Gers-Barlag, H., Gefeller, O., & Krutmann, J. (2004). Induction of the photoaging-associated mitochondrial common deletion in vivo in normal human skin. Journal of Investigative Dermatology, 122(5), 1277–1283. doi:10.1111/j.0022-202X.2004.22502.x
Katsuyama, Y., Yamawaki, Y., Sato, Y., Muraoka, S., Yoshida, M., Okano, Y., & Masaki, H. (2022). Decreased mitochondrial function in UVA-irradiated dermal fibroblasts causes the insufficient formation of type I collagen and fibrillin-1 fibers. Journal of Dermatological Science, 108(1), 22–29. doi:10.1016/j.jdermsci.2022.10.002
Kim, K. H., Son, J. M., Benayoun, B. A., & Lee, C. (2018). The mitochondrial-encoded peptide MOTS-c translocates to the nucleus to regulate nuclear gene expression in response to metabolic stress. Cell Metabolism, 28(3), 516–524.e7. doi:10.1016/j.cmet.2018.06.008
Lee, C., Zeng, J., Drew, B. G., et al. (2015). The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metabolism, 21(3), 443–454. doi:10.1016/j.cmet.2015.02.009
Oblong, J. E., Bowman, A., Rovito, H. A., et al. (2020). Metabolic dysfunction in human skin: Restoration of mitochondrial integrity and metabolic output by nicotinamide (niacinamide) in primary dermal fibroblasts from older aged donors. Aging Cell, 19(10), e13248. doi:10.1111/acel.13248
Vidali, S., Feichtinger, R. G., Emberger, M., et al. (2023). Ageing is associated with a reduction in markers of mitochondrial energy metabolism in the human epidermis. Experimental Dermatology, 32(6), 900–905. doi:10.1111/exd.14778