Showing posts with label skin. Show all posts
Showing posts with label skin. Show all posts

Monday, September 28, 2026

Breakthrough drug reverses aging in skin and dramatically speeds healing


A drug designed to eliminate worn out, aging cells may help older skin recover from injury much faster, according to research published in Aging (Aging-US). The work, titled "Topical ABT-263 treatment reduces aged skin senescence and improves subsequent wound healing," suggests that targeting "zombie cells" in the skin could one day improve healing after surgery, injury, or chronic wounds in older adults.



The research team included Maria Shvedova, Rex Jeya Rajkumar Samdavid Thanapaul, Joy Ha, Jannat Dhillon, Grace H. Shin, Jack Crouch, Adam C. Gower, Sami Gritli, and Daniel S. Roh from Boston University Aram V. Chobanian and Edward Avedisian School of Medicine.

Clearing Out Aging Cells

As skin gets older, damaged cells can accumulate instead of dying off. These cells, known as senescent cells, no longer work normally, but they remain active enough to interfere with nearby tissue. Over time, they can release inflammatory signals and other molecules that weaken the skin's ability to repair itself.

The researchers tested whether ABT-263, a senolytic drug, could reduce this burden when applied directly to aged skin. Senolytic drugs are designed to selectively remove senescent cells, which have been linked to aging, inflammation, and slower tissue repair.

In the study, aged mice received ABT-263 on their skin for five days. After treatment, the skin showed fewer signs of cellular aging. When the researchers then created small wounds, the treated mice healed more quickly than untreated mice.

By day 24, 80% of the mice treated with ABT-263 had fully healed wounds, compared with 56% of untreated mice.

A Surprising Healing Boost

One of the more unexpected findings was that ABT-263 briefly increased inflammation in the skin. In many cases, inflammation is seen as harmful, especially when it becomes chronic. But in this case, the short burst appeared to help prepare the skin for repair.

The treatment seemed to wake up healing pathways that are normally sluggish in older tissue. Gene activity increased in areas tied to wound repair, including collagen production, blood vessel growth, tissue remodeling, and other processes needed to close and strengthen damaged skin.

This matters because aging skin does not just wrinkle or thin. It also becomes less responsive after injury. That slower response can increase the risk of prolonged recovery after surgery, delayed closure of wounds, and complications in people with chronic skin injuries.

Why Topical Treatment Matters

ABT-263 has drawn interest because it can target senescent cells, but oral senolytic drugs may cause side effects because they circulate through the body. Applying the drug directly to the skin could offer a more focused approach.

In this study, topical ABT-263 reduced signs of senescence in aged mice, but it did not appear to have the same effect in young mice. That suggests the treatment may be most active in older tissue, where senescent cells have built up.

The researchers believe this targeted approach could be especially useful before surgery or in people at risk for poor wound healing. Instead of waiting for a wound to struggle, a treatment might one day help prepare older skin in advance.

"Our study underscores the potential of topical senolytic treatments to enhance wound healing in aging skin, presenting a potentially promising strategy for preoperative care."

Newer Research Points in the Same Direction

Since this 2024 work, the broader field has continued moving toward localized senolytic strategies for skin repair. A 2025 review in Ageing Research Reviews described cellular senescence as a key contributor to skin aging and skin disease, while noting that senolytics and related therapies could become useful tools for targeting harmful senescent cells in the skin.

A 2026 study took the idea further in diabetic wound healing, a major medical challenge often marked by chronic inflammation, poor blood vessel growth, and cellular senescence. Researchers developed a localized wound dressing carrying ABT-263 and reported that it reduced senescent cell burden, improved healing in diabetic mice, and showed no detectable systemic toxicity in that model.

At the same time, scientists are careful not to portray senescent cells as purely bad. A 2024 Frontiers in Immunology review emphasized that senescence can play a helpful role during normal wound repair, but persistent senescent cells may contribute to chronic wounds, fibrosis, and abnormal healing. The challenge is timing and precision: removing the harmful lingering cells without disrupting the useful early repair signals.

Promise With Important Caution

The findings are exciting, but they are still early. The ABT-263 skin study was done in mice, and more work is needed before scientists know whether the treatment is safe or effective in people.

Researchers will also need to answer key questions about dosing, timing, long term safety, and whether the benefits apply to human skin, surgical recovery, diabetic wounds, or other slow healing conditions.

Still, the idea is powerful. By clearing away cells that hold aging skin back, topical senolytic treatments could someday help the body repair itself more quickly and more effectively. For older adults facing surgery or chronic wounds, that could make healing less difficult, less risky, and far faster.


https://en.wikipedia.org/wiki/Navitoclax
https://www.aging-us.com/article/206165/text
Breakthrough drug reverses aging in skin and dramatically speeds healing |

Monday, December 30, 2013

Molecule critical to healing wounds identified

Skin provides a first line of defense against viruses, bacteria and parasites that might otherwise make people ill. When an injury breaks that barrier, a systematic chain of molecular signaling launches to close the wound and re-establish the skin's layer of protection. 

A study led by researchers from the University of Pennsylvania's School of Dental Medicine and published in the Journal of Cell Biology now offers a clearer explanation of the role of one of the players in the wound-healing process, a molecule called FOX01. Contrary to what had been expected, FOX01 is critical to wound healing, providing researchers with a possible new target for drugs that could help speed that process for people with impaired wound healing.
Senior author Dana Graves is a professor in Penn Dental Medicine's Department of Periodontics and is vice dean for scholarship and research. He collaborated on the study with Penn's Bhaskar Ponugoti, Fanxing Xu, Chenying Zhang, Chen Tian and Sandra Pacio.
A critical element of wound healing involves the movement of keratinocytes, the primary cells comprising the epidermis, or the outer layer of skin. Previous research had found that FOX01 was expressed at higher levels in wounds, but scientists did not understand what role the molecule was playing. In other scenarios, such as in cancer cells, FOX01 promotes cell death and interferes with the cell reproduction, two actions that would seem to be detrimental to healing.
To investigate the role of FOX01 in wound healing, Graves and colleagues bred mice that lacked the protein in their keratinocytes and then observed the wound healing process in these mice compared to mice with normal FOX01.
"We thought that deleting FOX01 would speed up the wound-healing process," Graves said, "but in fact it had the opposite effect."
The mice that lacked FOX01 showed significant delays in healing. Whereas all wounds on control mice were healed after one week, all of the experimental mice still had open wounds.
Digging deeper into this counterintuitive finding, the researchers examined the effect of reducing FOX01 levels on other genes known to play a role in cell migration. They found that many of these genes were significantly reduced, notably TGF-β1, a critical growth factor in wound repair. When the team added TGF-β1 to cells lacking FOX01, the cells behaved normally and produced the proper suite of molecules needed for healing, indicating that FOX01 acts upstream of TGF-β1 in the signaling pathway triggered during the healing process.
Further experimenting revealed that mice lacking FOX01 had evidence of increased oxidative stress, which is detrimental to wound healing.
"The wound healing environment is a stressful environment for the cell," Graves said. "It appears that upregulation of FOX01 helps protect the cell against oxidative stress."