Arresting cell cycles and the effect on wound healing.
Wounds that contain a significant number of fibroblasts that are arrested because of senescence, damaged DNA, or enduring quiescence do not heal. As the arrested population of cells decreases and more cells that divide and contribute to wound repair populate the wound, the wound is more likely to achieve closure. Having an understanding of the regulatory mechanisms within the cell cycle is important to wound repair, particularly chronic wounds. The theory of cellular senescence in chronic wounds is new and has never been tested. Studies seem to show that senescent cells in chronic wounds are a significant part of the wounding process. Senescence is irreversible, and senescent cells are refractory to growth factor therapy. Future growth factor therapies or genetic transfections that are capable of repairing the short circuit in cycling cells or overriding the senescent condition will be important partners in the successful treatment of chronic wound patients.
Vande Berg
Jerry S
JS
Core Clinical and Research Imaging Facility, V-151, San Diego Veterans Administration Medical Center, 3350 La Jolla Village Drive, San Diego, CA 92161, USA. jvandeberg@vapop.ucsd.edu
Robson
Martin C
MC
D002453:Cell Cycle / Q000502:physiology*; D018797:Cell Cycle Proteins / Q000502:physiology; D002908:Chronic Disease; D006801:Humans; D011183:Postoperative Complications; D013514:Surgical Procedures, Operative / Q000009:adverse effects*; D014945:Wound Healing / Q000502:physiology*; D014950:Wounds, Penetrating / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy*
D018797:Cell Cycle Proteins