Ординатура / Хирургия / @xirurgi_2025 / @xirurgi_2025 - 597 - файл

In animal models, pathological scars are either induced or human hypertrophic scar or keloid tis­sue is transplanted [3]. Despite the large number of studies describing pigs, mice, rabbits, and other animals as models to investigate hypertro­phic scarring or keloid formation, the basic skin physiology, immunology, and therefore the wound healing process are markedly different with the result that animals do not develop scars which are comparable with adverse scars in humans [19–22]. The implantation of human cells or tissue fragments of pathological scars into animal models has been reported to be more successful, resulting in a palpable nodule-like mass [3, 23]. Keloid and hypertrophic scar skin (full thickness or dermis only) can directly be grafted for example in nude mice models [19]. Also the transplantation of healthy human split­thickness skin grafts has been reported for the humanization of nude mouse models [20]. The greatly reduced number of T cells in these mice results in a reduced chance of graft rejection. However, the immune component of wound heal­ing and scar formation is severely compromised due to the immune-decient phenotype of this mouse model [6]. While implanted scar tissue is generally able to retain the pathological scar-spe­cic collagen even within animal models, the use of already established hypertrophic scar and keloid tissue does not allow the investigation of a de novo development [3]. To overcome this issue, Zhang etal. reported a combination of tissue cul­ture techniques with IL-6 and IL-17 exposure for the implantation of a keloid broblasts-hydrogel suspension into nude mice resulting in a de novo keloidal collagen formation [21].