Myeloid cell-specific sirtuin 6 deficiency delays wound healing in mice by modulating inflammation and macrophage phenotypes

Abstract

Wound healing: Protein deficiency hinders repair The loss of a protein involved in regulating white cell populations at wound sites can delay healing. Macrophages, a type of white blood cell, are crucial to wound healing. The M1 type of macrophage triggers initial inflammation, consumes damaged tissues, and secretes other molecules that help healing. M1 cells switch to the M2 type during the later stages of wound repair. Seok-Kweon Yun and Byung-Hyun Park at Chonbuk National University Medical School, Jeonju, South Korea, and co-workers examined macrophage phenotypes in wounds, focusing on a protein involved in macrophage type called sirtuin 6 (Sirt6). They compared wound healing responses in wild type mice and those without myeloid Sirt6. In myeloid Sirt6-deficient mice, increased levels of M1 macrophages induced higher levels of inflammation. There was also failure in M2 phenotypic switching in myeloid Sirt6 KO mice, which further delayed wound healing.