Oxidative stress and "senescent" fibroblasts in non-healing wounds as potential therapeutic targets.

In chronic wounds, fibroblast dysfunctions, such as increased apoptosis, premature senescence, senescence-like phenotype, or poor growth response in the absence of senescence markers, have been reported. Some of these differential dysfunctions may be secondary to differences in patient age or sex, ulcer size or duration, edge versus base sampling, or culture technique. Nevertheless, the entire spectrum of fibroblast dysfunction may exist and be secondary to, or a response to, different amounts of oxidative stress.