Diabetes Impedes the Epigenetic Switch of Macrophages into Repair Mode

Johanna A Knipper; Xiaolei Ding; Sabine A Eming

doi:10.1016/j.immuni.2019.07.009

Diabetes Impedes the Epigenetic Switch of Macrophages into Repair Mode

Immunity. 2019 Aug 20;51(2):199-201. doi: 10.1016/j.immuni.2019.07.009.

Authors

Johanna A Knipper¹, Xiaolei Ding², Sabine A Eming³

Affiliations

¹ Institute of Immunology and Infection Research, University of Edinburgh, Edinburgh EH9 3FL, UK.
² Department of Dermatology, University of Cologne, Kerpenerstr 62, 50937 Cologne, Germany.
³ Department of Dermatology, University of Cologne, Kerpenerstr 62, 50937 Cologne, Germany; Center for Molecular Medicine Cologne (CMMC), University of Cologne, 50931 Cologne, Germany; Cluster of Excellence Cellular Stress Responses in Aging-associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany. Electronic address: sabine.eming@uni-koeln.de.

PMID: 31433963
DOI: 10.1016/j.immuni.2019.07.009

Abstract

In this issue of Immunity, Kimball et al. (2019) show that restoring expression of the chromatin modifying enzyme Setdb2 in macrophages rescues impaired wound healing associated with type 2 diabetes. Their findings reveal epigenetic regulation as central to the resolution of macrophage-mediated inflammation in tissue repair and have therapeutic implications for the treatment of diabetic wounds.

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MeSH terms

Diabetes Mellitus, Type 2*
Epigenesis, Genetic
Histone Methyltransferases
Humans
Macrophages
Phenotype
Uric Acid
Wound Healing

Substances

Uric Acid
Histone Methyltransferases