Source: Columbia University Medical Center

Understanding the molecular mechanisms that facilitate growth within dormant hair follicles may seem like an endeavor rooted in the vanity of middle-aged men experiencing the genetic effects of male-patterned baldness. However, there are many skin disorders and autoimmune diseases where hair loss is an equally unwelcome and demoralizing symptom, for which there are few treatments.

Now, researchers from Columbia University Medical Center have discovered that inhibiting a family of enzymes inside resting hair follicles restores hair growth on mice and human hair follicles in vitro. Specifically, the investigators found drugs that inhibit the Janus kinase (JAK) family of enzymes, promoted rapid and robust hair growth when applied topically.

Interestingly, the study brings to the foreground the possibility that drugs commonly known as JAK inhibitors could be used to restore hair growth in multiple forms of hair loss. Currently, two JAK inhibitors have been approved by the U.S. Food and Drug Administration—one for the treatment of blood diseases (ruxolitinib) and the other for rheumatoid arthritis (tofacitinib). Both compounds are presently in clinical trials for the treatment of plaque psoriasis and alopecia areata, an autoimmune disease that causes hair loss.     

“What we've found is promising, though we haven't yet shown it is effective for male pattern baldness,” explained senior author Angela Christiano, Ph.D., associate professor of molecular dermatology at Columbia University Medical Center. “More work needs to be done to test formulations of JAK inhibitors specially made for the scalp to determine whether they can induce hair growth in humans.”

The findings from this study were published online recently in Science Advances through an article entitled “Pharmacologic inhibition of JAK-STAT signaling promotes hair growth.”

As happens so often in biomedical research, Dr. Christiano and her team serendipitously stumbled upon the effect of JAK inhibitors on hair follicles while they were studying alopecia areata, which is caused by autoimmune attack on the hair follicles. The Columbia team previously noticed that JAK inhibitors shut off the signal that provokes the autoimmune attack, and that oral forms of the drug restore hair growth in some people with the disorder.

Additionally, the researchers found that mice grew more hair when the drug was applied topically to the skin than when given internally—suggesting that JAK inhibitors might have a direct effect on the hair follicles in addition to inhibiting the immune attack.

What Dr. Christiano’s team found was JAK inhibitors rapidly awakened resting follicles out of their resting phase, called telogen, and successfully modulated their entry into the growth phase, which is termed anagen. Mice treated for five days with one of two JAK inhibitors sprouted new hair within ten days, greatly accelerating the hair follicle growth phase. Conversely, hair growth was not observed untreated control mice during the same period.

“There are very few compounds that can push hair follicles into their growth cycle so quickly,” noted Dr. Christiano. “Some topical agents induce tufts of hair here and there after a few weeks, but very few have such a potent and rapid-acting effect.” The drugs also produce longer hair from human hair follicles grown in culture and on skin grafted onto mice.

Dr. Christiano and her team are excited by their initial findings and hope that the use of JAK inhibitors will open up new avenues of research into the regrowing of hair. However, the team is quick to point out that it remains to be seen if JAK inhibitors can reawaken hair follicles that have been suspended in a resting state because of androgenetic alopecia (the cause of male and female pattern baldness) or other forms of hair loss, as the current study was done on normal mice and human follicles.

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