The wound healing in the human body occurs through a series of stages called hemostasis, inflammation, proliferation and remodeling as described on the home page. These stages consist of their own characteristics and each have a specific role in the healing of such wounds. If some of the processes in wound healing were to occur incorrectly, such as fibroblast migration or the formation of epithelium, it may lead to disorders or deformations of the wounds. We experience this wound healing process quite often in our lives, whether we scrape our knees or get a paper cut, which is why it is important to gain a better understanding of what takes place when these injuries heal. Understanding the role of ceramide kinase, the enzyme that promotes the production of ceramide-1-phosphate, may spark insight on how to treat larger, abnormal healing processes that may lead to disorders.

Investigating enzymes or other molecules that are involved in each stage of the whole process will pinpoint exactly how the process may go wrong and what movements are needed in order for it to happen correctly instead. Wijesinghe et. al. 2014 dove deeper into such components, especially the enzyme ceramide kinase and its role in the migratory properties of fibroblasts.

Fibroblast migration occurs when the fibroblasts travel to the wound site toward the end of the inflammation stage of wound healing. One way this happens is when eicosanoids, signaling molecules created by the cytosolic phospholipase A₂-induced production of arachidonic acid, bind to the cell membrane receptors of fibroblasts. This binding causes internal signaling that induces the migration of these fibroblasts. Ceramide-1-phosphate, the production of which is promoted by ceramide kinase, activates cytosolic phospholipase A₂ and increases the time cPLA₂ is active in the membrane. This increases arachidonic acid production and release of arachidonic acid outside of the membrane. Does the genetic ablation of ceramide kinase affect the arachidonic acid release and migration patterns of fibroblasts? Is ceramide kinase an obvious influencer in the proper healing of wounds through fibroblast migration to the wound site?