Skin wounds are notoriously difficult to heal, and they can take months or even years to close.
Researchers from Washington University School of Medicine in St. Louis and Northwestern University Feinberg School of Medicine have discovered a process that causes damaged skin cells to close too quickly over wounds, which might explain why some patients have persistent wound issues.
The findings were published in the journal Nature Communications on March 28.
However recent discoveries may completely change the game up in relation to wound healing.
Scientists Discover a New Mechanism that Promotes Wound Healing in Skin Cells
- A novel biochemical route that enhances skin wound healing has been discovered by researchers at the University of California, Irvine.
- The work was published today in JCI Insight under the title “GRHL3 triggers FSCN1 to relax cell-cell adhesions between migratory keratinocytes during wound reepithelialization.”
- GRHL3 loosens the adhesion between injured skin cells during wound healing by activating a protein-coding gene called Fascin Actin-Bundling Protein 1 (Fscn1), according to the study.
- Researchers have discovered that changes in this mechanism can lead to chronic, non-healing lesions like diabetic ulcers, which afflict millions of people each year.
What’s intriguing about our results is that we’ve found a molecular pathway that is active in normal acute wounds in people and changed in diabetes wounds in mice.Dr. Ghaidaa Kashgari, Ph.D.- a postdoctoral researcher in the Department of Medicine at the University of California, Irvine.
Dr. Kashgari followed on to say the result had substantial therapeutic implications and that it might help us better understand wound healing biology.
Acute wounds usually heal in a predictable and efficient way, moving through four separate but overlapping stages of wound healing: hemostasis, inflammation, proliferation, and remodeling.
Chronic wounds, on the other hand, will begin to heal in the same way but will go through longer inflammatory, proliferative, or remodeling stages, culminating in tissue fibrosis and non-healing ulcers.
Four Wound healing is a complicated process that involves a wide range of specialized cells, including platelets, macrophages, fibroblasts, epithelial, and endothelial cells.
These cells communicate with one another as well as with the extracellular matrix.
Healing is controlled by the activity of proteins and glycoproteins including cytokines, chemokines, growth factors, inhibitors, and their receptors, in addition to the numerous cellular connections.
There are specific thresholds that must be met at each stage of wound healing in order for normal healing to proceed.
It is necessary to evaluate the healing process in normal wounds in order to determine the variations present in chronic wounds that impede recovery.
Keratinocytes, the cells that make up the skin’s outer layers, relocate on top of the underlying granulation tissue, which is the uneven, pink tissue that develops around the margins of a wound, during reepithelialization.
To seal the incision, the keratinocytes eventually meet migratory keratinocytes from the opposite edge.
“Despite considerable advancements in therapy, plenty remains unknown about the molecular pathways underlying normal wound healing,” stated lead author Bogi Andersen, MD, of the UCI School of Medicine’s Departments of Biological Chemistry and Medicine, Division of Endocrinology.
“Our findings show how anomalies in the GRHL3/FSCN1/E-cadherin pathway may play a role in non-healing wounds, and this needs to be explored further.”
To Wrap Things Up
Wound healing is a dynamic and complicated process that involves the replacement of devitalized and missing microstructures and tissue layers.
The wound healing process in adults can be split into three or four different phases.
Some writers argue that there are three phases: inflammatory, fibroblastic, and maturation, which have alternatively been referred to as inflammatory, proliferation, and remodeling.
The hemostasis phase, the inflammatory phase, the proliferation phase, and the remodeling phase are the four phases of the four-phases concept.
The hemostasis phase is contained inside the inflammatory phase in the three-phases method.
Experts vary not just in the phased approach they employ, but also in the phase pejoratives they use; they may call phases the hemostasis phase, inflammatory phase, proliferation phase, and remodeling phase, or the hemostasis phase, inflammatory phase, granulation phase, and maturation phase.
As a result, several phases, such as remodeling or maturation, and proliferation of granulation, have multiple names. The National Institutes of Health and the Irving Weinstein Foundation funded this research.