| First Author | Kita A | Year | 2022 |
| Journal | Commun Biol | Volume | 5 |
| Issue | 1 | Pages | 310 |
| PubMed ID | 35383267 | Mgi Jnum | J:323946 |
| Mgi Id | MGI:7263515 | Doi | 10.1038/s42003-022-03266-3 |
| Citation | Kita A, et al. (2022) Altered regulation of mesenchymal cell senescence in adipose tissue promotes pathological changes associated with diabetic wound healing. Commun Biol 5(1):310 |
| abstractText | Pathologic diabetic wound healing is caused by sequential and progressive deterioration of hemostasis, inflammation, proliferation, and resolution/remodeling. Cellular senescence promotes wound healing; however, diabetic wounds exhibit low levels of senescent factors and accumulate senescent cells, which impair the healing process. Here we show that the number of p15(INK4B) + PDGFRalpha + senescent mesenchymal cells in adipose tissue increases transiently during early phases of wound healing in both non-diabetic mice and humans. Transplantation of adipose tissue from diabetic mice into non-diabetic mice results in impaired wound healing and an altered cellular senescence-associated secretory phenotype (SASP), suggesting that insufficient induction of adipose tissue senescence after injury is a pathological mechanism of diabetic wound healing. These results provide insight into how regulation of senescence in adipose tissue contributes to wound healing and could constitute a basis for developing therapeutic treatment for wound healing impairment in diabetes. |
