Diabetes Drug Could Prevent Scarring Through Targeting Fibroblasts
Scientists have long wondered the necessity of scars to the body’s healing process; when we are injured, why can’t our skin just regenerate back to the way it looked previously? Why do we have to carry such an unsightly reminder of the past, sometimes in visible places we don’t want others to see?
While some may see scars as the symbol of the healing process, others see them as a cosmetic burden. Does our body need scars to heal, or can we do without them without risks of infections or wounds reopening?
In a new study published in the journal Science, Dr. Michael Longaker, co-director of the Institute for Stem Cell Biology and Regenerative Medicine at Stanford University, sought to uncover the mystery behind scars, and whether they are necessary. By deciphering the specific molecular steps involved in the scarring process, Longaker was able to discover a way of preventing them from forming.
His research started during an observation at the beginning of his career as a plastic surgeon; while operating on fetuses still in the womb, he found that no matter what kind of incisions the surgeon made, the fetuses did not scar. He began to wonder, if fetuses do not scar, then why do babies once they are born?
He then took his research to the lab, examining two different types of fibroblasts, or cells responsible for maintaining structures of organs and tissues, within mice. He and his team honed in on one type of fibroblast, primarily involved in wound healing, as well as forming tumors like melanoma. Longaker tells Time, “This type of fibroblast starts out as less than one percent of the developing skin, but by the time an animal is a month old, it’s 80 percent of the fibroblasts in skin on the back of the animal.”
In order to kill off these fibroblasts, Longaker administered diphtheria toxin to his mice and found they scarred less. He also discovered that these fibroblasts possess a marker on their surface that makes them easy to detect, and thus eliminate. Longaker’s final and most fortunate finding was that there is a type 2 diabetes drug currently on the market that works in a similar way to diphtheria toxin to inhibit fibroblasts’ markers and ultimately stop scarring.
Researchers tested this drug on their mice, finding that it did reduce scarring without compromising the integrity of the tissue and making it more susceptible to reopening. This is particularly promising, especially since 80 million operations occur in the US each year, along with the countless scars people receive from accidents on their own. This drug may also help those who develop fibrous tissue after receiving cancer-fighting radiation treatment. Longaker believes that if this drug is used before wounds begin to heal, there is little chance a scar will not develop.
Researchers are not sure of the applicability of this treatment to already existing scars, but believe doctors will be more willing to do revision surgery to reduce the appearance of scars if this type of drug exists. Researchers are also hopeful that this treatment may extend beyond cosmetics to be used medically for heart attacks, as well as for spinal cord injuries in tissues receiving radiation.
Source: Graham G, Hu M, Longaker M, et al. A Scar is Born: Origins of Fibrotic Skin Tissue. Science. 2015.