A survey directed by NYU School of Medicine researchers, in consultation with the Wound Healing Program at Columbia University, sheds new light on the molecular mechanisms underlying the growth of chronic wounds. The findings may help clinicians foretell which wounds are likely to become chronic -- a key bit of info, since the earlier treatment is started, the better the result. The research also raises the hope for new interventions for chronic wounds by identifying possible targets for intervention.
Chronic wounds, which includes bedsores, are a ordinari and potentially grave problem, typically occurring in people with diabetes or poor circulation, older people, and anyone who is bedridden or wheelchair-bound. Bedsores -- alias bedsore or pressure ulcers -- have been estimated to affect about five to tenth of hospital patients, 13 percent of home residents, and up to 39 percent of spinal cord injury patients in the United States.
Chronic injuries oftentimes leads to far flung infections and limb amputations, says Marjana Tomic-Canic, Ph.D., Associate Professor of Dermatology and Microbiology at NYU School of Medicine, the study's lead author.
Examining tissue taken from chronic wounds in humans, the researchers observed that skin cells get stuck in the middle of the normal healing process and can not transmigrate to the wound site. The stalling of the healing procedure, the researchers discovered, is caused by excess of a molecule called c-myc (a product of the ubiquitous myc gene, which has been implicated in many human cancers). This molecule is known to subdue cell migration and to cause the skin to thicken, obstructing reparative cells from reaching the edge of the wound.
The cause of c-myc overproduction was then followed one step up the molecular tract to beta-catenin, a critical governor of cell behaviour. According to the researchers, beta-catenin activates the production of c-myc as well as other pathways that affect the migration, growth, and regulation of skin cells.
Chronic wounds, which includes bedsores, are a ordinari and potentially grave problem, typically occurring in people with diabetes or poor circulation, older people, and anyone who is bedridden or wheelchair-bound. Bedsores -- alias bedsore or pressure ulcers -- have been estimated to affect about five to tenth of hospital patients, 13 percent of home residents, and up to 39 percent of spinal cord injury patients in the United States.
Chronic injuries oftentimes leads to far flung infections and limb amputations, says Marjana Tomic-Canic, Ph.D., Associate Professor of Dermatology and Microbiology at NYU School of Medicine, the study's lead author.
Examining tissue taken from chronic wounds in humans, the researchers observed that skin cells get stuck in the middle of the normal healing process and can not transmigrate to the wound site. The stalling of the healing procedure, the researchers discovered, is caused by excess of a molecule called c-myc (a product of the ubiquitous myc gene, which has been implicated in many human cancers). This molecule is known to subdue cell migration and to cause the skin to thicken, obstructing reparative cells from reaching the edge of the wound.
The cause of c-myc overproduction was then followed one step up the molecular tract to beta-catenin, a critical governor of cell behaviour. According to the researchers, beta-catenin activates the production of c-myc as well as other pathways that affect the migration, growth, and regulation of skin cells.
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